Image processing can cause some malignant soft-tissue lesions to be missed in digital mammography images.

AIM: To investigate the effect of image processing on cancer detection in mammography. METHODS AND MATERIALS: An observer study was performed using 349 digital mammography images of women with normal breasts, calcification clusters, or soft-tissue lesions including 191 subtle cancers. Images underwent two types of processing: FlavourA (standard) and FlavourB (added enhancement). Six observers located features in the breast they suspected to be cancerous (4,188 observations). Data were analysed using jackknife alternative free-response receiver operating characteristic (JAFROC) analysis. Characteristics of the cancers detected with each image processing type were investigated. RESULTS: For calcifications, the JAFROC figure of merit (FOM) was equal to 0.86 for both types of image processing. For soft-tissue lesions, the JAFROC FOM were better for FlavourA (0.81) than FlavourB (0.78); this difference was significant (p=0.001). Using FlavourA a greater number of cancers of all grades and sizes were detected than with FlavourB. FlavourA improved soft-tissue lesion detection in denser breasts (p=0.04 when volumetric density was over 7.5%) CONCLUSIONS: The detection of malignant soft-tissue lesions (which were primarily invasive) was significantly better with FlavourA than FlavourB image processing. This is despite FlavourB having a higher contrast appearance often preferred by radiologists. It is important that clinical choice of image processing is based on objective measures.

Validation of simulation of calcifications for observer studies in digital mammography.

Studies using simulated calcifications can be performed to measure the effect of different imaging factors on calcification detection in digital mammography. The simulated calcifications must be inserted into clinical images with realistic contrast and sharpness. MoCa is a program which modifies the contrast and sharpness of simulated calcification clusters extracted from images of mastectomy specimens acquired on a digital specimen cabinet at high magnification for insertion into clinical mammography images. This work determines whether the use of MoCa results in simulated calcifications with the correct contrast and sharpness. Aluminium foils (thickness 0.1-0.4 mm) and 1.60 µm thick gold discs (diameter 0.13-0.8 mm) on 0.5 mm aluminium were imaged with a range of thicknesses of polymethyl methacrylate (PMMA) using an amorphous selenium direct digital (DR) system and a powder phosphor computed radiography (CR) system (real images). Simulated images of the tests objects were also generated using MoCa. The contrast of the aluminium squares and the degradation of the contrast of the gold discs as a function of disc diameter were compared in the real and simulated images. The average ratios of the simulated-to-real aluminium contrasts over all aluminium and PMMA thicknesses were 1.03 ± 0.04 (two standard errors in the mean) and 0.99 ± 0.03 for the DR and CR systems, respectively. The ratio of the simulated-to-real degradations of contrast averaged over all disc diameters and PMMA thicknesses were 1.007 ± 0.008 and 1.002 ± 0.013 for DR and CR, respectively. The use of MoCa was accurate within the experimental errors.

Comparison of the x-ray attenuation properties of breast calcifications, aluminium, hydroxyapatite and calcium oxalate.

Aluminium is often used as a substitute material for calcifications in phantom measurements in mammography. Additionally, calcium oxalate, hydroxyapatite and aluminium are used in simulation studies. This assumes that these materials have similar attenuation properties to calcification, and this assumption is examined in this work. Sliced mastectomy samples containing calcification were imaged at ×5 magnification using a digital specimen cabinet. Images of the individual calcifications were extracted, and the diameter and contrast of each calculated. The thicknesses of aluminium required to achieve the same contrast as each calcification when imaged under the same conditions were calculated using measurements of the contrast of aluminium foils. As hydroxyapatite and calcium oxalate are also used to simulate calcifications, the equivalent aluminium thicknesses of these materials were also calculated using tabulated attenuation coefficients. On average the equivalent aluminium thickness was 0.85 times the calcification diameter. For calcium oxalate and hydroxyapatite, the equivalent aluminium thicknesses were 1.01 and 2.19 times the thickness of these materials respectively. Aluminium and calcium oxalate are suitable substitute materials for calcifications. Hydroxyapatite is much more attenuating than the calcifications and aluminium. Using solid hydroxyapatite as a substitute for calcification of the same size would lead to excessive contrast in the mammographic image.

Effects of BHV-1 on PMN adhesion to bovine lung endothelial cells.

Bovine herpes virus-1 (BHV-1) infection appears to decrease the rate of polymorphonuclear leukocyte (PMN) influx into the lung in response to the secondary invader, Pasteurella haemolytica. It was postulated that BHV-1 may affect the rate of cellular infiltration by altering the function of the endothelium, thereby preventing PMN movement across the blood-tissue barrier. Therefore, we decided to investigate the effect of BHV-1 on the ability of PMN to adhere to lung endothelial cells (LEC). LEC were isolated from fetal bovine fetal tissue and were shown to function in PMN adhesion assays. Furthermore, enhanced PMN adhesion was observed after exposure of LEC to recombinant bovine TNF-alpha (rBoTNF-alpha) for 4, 8, 12, and 24 h. LEC infected with BHV-1 were shown to be less responsive to rBoTNF-alpha. However, infection of LEC with BHV-1 at an multiplicity of infection (MOI) of 1.0 or 10 did not affect basal levels of PMN adhesion to these cells. Decreased PMN binding to BHV-1-infected LEC, simultaneously treated with rBoTNF-alpha, was observed at 10-12 h post-infection. The data suggest that BHV-1 may prevent cytokine-induced PMN infiltration of the lung through the modification of EC responses to cytokines.