Radiation dose to multidisciplinary staff members during complex interventional procedures.

INTRODUCTION: Complex interventional radiology procedures involve extensive fluoroscopy and image acquisition while staff are in-room. Monitoring occupational radiation dose is crucial in optimization. The purpose was to determine radiation doses received by staff involved in complex interventional procedures performed in a dedicated vascular or neuro intervention room. METHODS: Individual real-time radiation dose for all staff involved in vascular and neuro-interventional procedures in adult patients was recorded over a one-year period using wireless electronic dosimeters attached to the apron thyroid shield. A reference dosimeter was attached to the C-arm near the tube housing to measure scattered, unshielded radiation. Radiology staff carried shoulder thermo-luminescent dosimeters with monthly read-out to monitor dose over time. RESULTS: Occupational radiation dose was measured in 99 interventional procedures. In many cases prostate artery embolization procedures exposed radiologists to high radiation doses with a median of 15.0 µSv and a very large spread, i.e. 0.2-152.5 µSv. In all procedures except uterine fibroid embolization radiographers were exposed to lower doses than those of radiologists, with endovascular aortic repair being the procedure with highest median exposure to assisting radiographers, i.e. 2.2 µSv ranging from 0.1 to 36.1 µSv. Median radiation dose for the reference dosimeter was 670 µGy while median staff dose for all procedures combined was 3.2 µGy. CONCLUSION: Radiation doses for multiple staff were determined and the ratio between staff dose and reference dosimeter indicated proper use of shielding in general. Some high-dose procedures may need further optimization for certain staff members, especially those not primarily employed in radiology. IMPLICATIONS FOR PRACTICE: The study provides benchmark doses that may be used widely in audits and in the ongoing effort to optimize radiation protection for staff in interventional radiology.

Can advanced edge enhancement software improve image quality to visualise tubes, catheters and wires in digital chest radiographs?

INTRODUCTION: This study aimed to test whether Advanced Edge Enhancement (AEE) software could improve the localisation of tubes, catheters or wires, while also affecting the overall image quality in chest x-rays (CXR). METHODS: In total, 50 retrospective CXRs were included. All images were obtained utilising the Canon X-ray system (CANON/Arcoma Precision T3 DR System, Canon Europe, Amsterdam, NL) with a CXDI-810C wireless detector. A clinical image, plus three additional AEE algorithms were applied using post processing (two intensity variations 1 and 4) on all CXRs totalling 350 different images. Three radiologists evaluated the images using a subjective Absolute Visual Grading Analysis (VGA). The clinical images used in post processing were not applied as reference in the analysis. Each radiologist graded the images separately in a randomized order, with a score of three indicating suitability for diagnostic assessment. RESULTS: The three AEE algorithms contributed to an overall improvement (average 16-49%) in visualisation of tube, catheter or wire on CXR images. The Mann-Whitney U tests showed a statistically significant (p < 0.05) improvement in contrast resolution and sharpness, indicating an increased ability to differentiate tubes, wires or catheters tips from surrounding tissues. For the noise criterion, not applying any AEE algorithm showed a significantly higher homogeneity in soft tissue (p < 0.001), reducing the ability to visualise soft tissue. The high-intensity catheter algorithm was the only algorithm to achieve a statistically significant (p = 0.017) increase in the ability to differentiate pulmonary tissues of similar density. CONCLUSION: An overall improvement in the visualisation of tube, catheter and wire placement was obtained using the three AEE-algorithms. The bone and catheter algorithms showed the highest consistency, with the small structure algorithm underperforming in resolution and low contrast resolution. In general, image noise increased regardless of algorithm type or applied intensity. The AEE-algorithms should therefore be seen as a supplementary tool to the clinical image protocol, while having the potential to improve image quality to specific clinical situations. IMPLICATIONS FOR PRACTICE: AEE filtered images appear to be a supplement to the current practice of using CXRs in the diagnosis in placement of catheters, tubes and wires in the chest region. The use of AEE-algorithms has the potential to improve the daily work in clinical practice, which serves the basis for further investigation of its effect on radiographic practices.

Significant linkage to chromosome 12q24.32-q24.33 and identification of SFRS8 as a possible asthma susceptibility gene.

BACKGROUND: Asthma is a complex genetic disorder. Many studies have suggested that chromosome 12q harbours a susceptibility gene for asthma and atopy. Linkage on chromosome 12q24.21-q24.33 was investigated in 167 Danish families with asthma. METHODS: A two step procedure was used: (1) a genome-wide scan in one set of families followed by (2) fine scale mapping in an independent set of families in candidate regions with a maximum likelihood score (MLS) of > or =1.5 in the genome-wide scan. Polymorphisms in a candidate gene in the region on 12q24.33 were tested for association with asthma in a family based transmission disequilibrium test. RESULTS: An MLS of 3.27 was obtained at 12q24.33. The significance of this result was tested by simulation, resulting in a significant empirical genome-wide p value of 0.018. To our Knowledge, this is the first significant evidence for linkage on chromosome 12q, and suggests a candidate region distal to most previously reported regions. Three single nucleotide polymorphisms in splicing factor, arginine/serine-rich 8 (SFRS8) had an association with asthma (p < or = 0.0020-0.050) in a sample of 136 asthmatic sib pairs. SFRS8 regulates the splicing of CD45, a protein which, through alternative splice variants, has an essential role in activating T cells. T cells are involved in the pathogenesis of atopic diseases such as asthma, so SFRS8 is a very interesting candidate gene in the region. CONCLUSIONS: Linkage and simulation studies show that the very distal part of chromosome 12q contains a gene that increases the susceptibility to asthma. SFRS8 could act as a weak predisposing gene for asthma in our sample.

Facilitated transport of 3-O-methyl-D-glucose in human polymorphonuclear leukocytes.

Transport of the nonmetabolizable hexose analogue 3-O-methyl-D-glucose (30MG) was measured in human polymorphonuclear leukocytes at 37 degrees C, pH 7.4. 3OMG at very low concentration (0.05 mM) equilibrated with the intracellular water with a rate constant of about 0.08 s-1. Transport of 3OMG in the presence of 20 microM cytochalasin B and transport of L-glucose were insignificant. Countertransport of 14C-labelled 3OMG was demonstrated. Exchange of 3OMG between the extracellular and intracellular water showed saturation with a Km of about 4 mM. Thus, the transport of 3OMG is mediated almost exclusively by facilitated diffusion.

The effect of catecholamines and adenosine deaminase on the glucose transport system in rat adipocytes.

2-Deoxyglucose uptake (3 min) and 3-O-methylglucose transport (2 s) was measured in rat adipocytes preincubated with 5 microM epinephrine plus adenosine deaminase as described by Green (Green, A. (1983) FEBS Lett. 152, 261-264). 2-Deoxyglucose uptake was about 95% depressed in insulin-treated, but not in 'basal', cells preincubated with epinephrine plus adenosine deaminase for 60 min in broad agreement with Green's report. However, this depression was caused by a decrease in sugar phosphorylation rather than transport. In similarly incubated cells, transport of 3-O-methylglucose, a sugar analogue not phosphorylated in the adipocytes, was not affected by catecholamine plus adenosine deaminase. However, a decrease in transport of about 60% was observed both in the absence and the presence of insulin when the albumin concentration was high enough and the cell concentration low enough to prevent accumulation of free fatty acids in the medium. In addition, the insulin sensitivity with regard to hexose transport was markedly reduced. Transport was approximately doubled in cells incubated with 5 microM epinephrine in the absence of adenosine deaminase. Thus, epinephrine at a high concentration stimulates hexose transport in the absence of adenosine deaminase (presence of adenosine) whereas it inhibits both basal and insulin-stimulated transport in the presence of adenosine deaminase (absence of adenosine).

Cell association and degradation of alpha 2-macroglobulin-trypsin complexes in hepatocytes and adipocytes.

125I-Labelled alpha 2-macroglobulin-trypsin complex (125I-labelled alpha 2-macroglobulin X trypsin) was associated to isolated rat adipocytes and hepatocytes with a half-time of about 60 min at 37 degrees C. The association of 0.5 micrograms/ml 125I-labelled alpha 2-macroglobulin X trypsin was inhibited by unlabelled alpha 2-macroglobulin X trypsin with a half-inhibition constant of about 8 micrograms/ml (11 nM). 125I-Labelled alpha 2-macroglobulin became cell-associated to a smaller extent (10-40% of that of alpha 2-macroglobulin X trypsin) and the half-inhibition constant was about 35 micrograms/ml in adipocytes. The cell association of 125I-labelled alpha 2-macroglobulin X trypsin was markedly inhibited by dansylcadaverine, bacitracin, omission of Ca2+ from the medium or pretreatment of the cells with trypsin. After incubation for 180 min more than 60% of the cell-associated 125I-labelled alpha 2-macroglobulin X trypsin was not removed by treatment of the cells with trypsin-EDTA and represented probably internalized material. 125I-Labelled alpha 2-macroglobulin X trypsin was degraded to trichloroacetic acid-soluble fragments by suspensions of both cell types but only to a negligible extent by incubation media preincubated with these cells. The rate of degradation of 0.5 micrograms/ml 125I-labelled alpha 2-macroglobulin was approx. 40% of that of 125I-labelled alpha 2-macroglobulin X trypsin. Degradation of 125I-labelled alpha 2-macroglobulin X trypsin was abolished by a high concentration (0.5 mg/ml) of alpha 2-macroglobulin X trypsin. It is concluded that alpha 2-macroglobulin X trypsin by a specific and saturable mechanism is bound to, internalized and degraded by isolated rat adipocytes and hepatocytes.

Monoiodoinsulin labelled in tyrosine residue 16 or 26 of the B-chain or 19 of the A-chain. II. Characterization of the kinetic binding constants and determination of the biological potency.

The binding affinity to insulin receptors in isolated rat adipocytes at 37 degrees C of the four isomers of [125I]monoiodoinsulin was ranked as B26 greater than B16 = A14 greater than A19. It was demonstrated that the difference in affinity was mainly due to a change in the association rate constant, rather than in the dissociation rate constant. At steady state in the binding process the fraction of cell-associated 125I-activity eluting from a Sephadex G-50 Fine column at a position identical to that of iodoinsulin was greater than 90% and independent of the position of the iodine. It was also shown that the formation of [125I]-monoiodotyrosine as a consequence of receptor-mediated degradation was proportional to the respective binding affinities of the four isomers. The two isomers with binding affinities different from that of [A14-Tyr-125I]monoiodoinsulin (i.e. the B26 and the A19 isomers, respectively) were shown to have biological potencies which corresponded within +/- 8% to the observed changed binding affinities. In cultured human lymphocytes of the IM-9 line the hierarchy of binding affinities at 37 degrees C was B26 greater than B16 greater than A14 greater than A19, and in cultured human colon adenocarcinoma cells of the HT-29 line the binding affinities were ranked in the order B26 greater than B16 greater than A14 greater than or equal to A19 indicating that the functional properties of the insulin receptor vary within cell types and/or species.

[Growth hormone and Somatomedin. A brief review (author's transl)]. / Vaeksthormon og Somatomedin. En kort oversigt

In addition to a direct effect on the metabolic processes of several tissues (table I) growth hormone exerts the functions of a classical trophic hypophyseal hormone by stimulating the synthesis of a secondary hormone. This hormone, Somatomedin, is a growth promoting hormone with cartilage and connective tissues as specific target organ. The activity of somatomedin in plasma changes with the concentration of growth hormone both at the physiological level (constitutional differences in growth rate, fig. 2) and at the pathological level (acromegaly/pituitary dwarfism). The connection between growth hormone and somatomedin at different nutritional conditions is, however, not clearcut. The organ of production of somatomedin, a peptide hormone of ca. 6000 Dalton, is not yet known.