Ductography: how to and what if?

Ductography of the breast is an underused procedure that often helps define the cause of unilateral, single-pore, spontaneous nipple discharge. Since nipple discharge may be caused by benign tumors, such as papillomas, or by carcinoma, such as ductal carcinoma in situ, identification of intraductal abnormalities with ductography is important. Further, diagnostic ductography and preoperative ductography help guide accurate surgical intervention. Without prior ductography, central duct excision may not result in removal of the abnormal ductal tissue or may result in removal of only a portion of the abnormal ductal system, causing the extent of disease to be effectively understaged. Once fundamental ductographic principles are learned, the procedure is easy to perform. If extravasation occurs, ductography is rescheduled for 7-14 days later. Elimination of air bubbles from the cannula, syringe, and extension tubing is vital. When reflux occurs, radiologists must be aware of a possible tumor in the distal-most duct. When ductal ectasia or fibrocystic changes are the cause of the discharge, conservative follow-up may be considered. Diagnostic radiologists who learn the technique of ductography and include it in their evaluation of nipple discharge will improve their interdisciplinary approach to this important sign of breast cancer.

Breast cancer diagnosis using scattered X-rays.

Small-angle X-ray diffraction data has been collected from 99 ;core-cut' breast tissue specimens representing a number of different pathologies. Data in the range 75-1390 A have been compared with controls from patients with no breast disease. Bessel functions and Bragg maxima resulting from the fibrillar structure of collagen have been identified. The Bragg maxima indexed onto a 649 A lattice. Systematic differences in the intensities and D-spacings between the collagen of malignant, benign and normal tissue groups have been clearly demonstrated and quantified. These differences appear to be due to a significantly lower structural order within the malignant tissues. Possible explanations for this are discussed and the potential for utilizing this observation in cancer diagnosis is considered.

Cardiac MRI of the normal and hypertrophied mouse heart.

With the development of recent transgenic techniques, studies involving mice offer opportunities to increase understanding of cardiac disease. This provides motivation for the current study to perform noninvasive evaluation of the normal and hypertrophied mouse heart with MRI. By acquiring ECG and respiratory signals, the MR image acquisition was gated to both the cardiac and respiratory cycles. Combining a spin-warp imaging sequence with an RF surface coil resulted in short-axis images that allowed quantification of in vivo cardiac mass. Excellent agreement between MRI-determined (y) and postmortem heart weight (x) was obtained: y = 0.991x + 1.43 (r = 0.996). Isoproterenol, at 282 micromol/kg body weight (BW) and 573 micromol/kg BW, induced a dose-dependent increase in the ratio of heart weight to BW of 16.8 +/- 1.09% and 24.1 +/- 1.71%, respectively, which was accurately measured by MRI. These results demonstrate the ability of MRI to noninvasively monitor cardiac anatomy in the mouse.

Dilated cardiomyopathy in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-alpha.

The failing human heart expresses tumor necrosis factor-alpha (TNF-alpha). However, its pathophysiological significance is not clear. We previously reported that robust overexpression of TNF-alpha in the murine heart causes lethal myocarditis. In this study, we modified the transgene to reduce the production of TNF-alpha by preserving the destabilizing sequence in TNF-alpha cDNA. Expression was driven by the murine alpha-myosin heavy chain promoter. Use of this modified construct allowed to the establish a mutine transgenic line (TG). TG offspring were examined at 6, 12, and 24 weeks. All showed a significantly higher heart weight-to-body weight ratio. Northern blot analysis confirmed the expression of transgene in the heart, and enzyme-linked immunosorbent assay demonstrated the presence of TNF-alpha protein. The TG heart demonstrated a mild, diffuse, lymphohistiocytic interstitial inflammatory infiltrate. Cardiomyocyte necrosis and apoptosis were present but not abundant. Magnetic resonance imaging showed that the TG heart was significantly dilated with reduced ejection fraction. Although the left ventricular dP/dtmax was not different at baseline, its responsiveness to isoproterenol was significantly blunted in TG. Atrial natriuretic factor was expressed in the TG ventricle. A group of TG died spontaneously, and subsequent autopsies revealed exceptional dilation of the heart, increased lung weight, and pleural effusion, suggesting that they died of congestive heart failure. The cumulative mortality rate at 6 months was 23%. In conclusion, the mouse overexpressing TNF-alpha recapitulated the phenotype of congestive heart failure. This provides a novel model to elucidate the role of this cytokine in the development of congestive heart failure.

The radiology of total shoulder replacement.

The indications for total shoulder replacement and the radiologic evaluation prior to the operation are discussed in depth in this article. Different approaches to clinical problems are also discussed and illustrated, as are normal findings. This is followed by a discussion of the complications of shoulder reconstruction, including infection, fractures, and heterotopic bone formation. A review of the results is also given followed by a brief mention of a number of other orthopedic shoulder devices and plates.