Background-Duchenne muscular dystrophy (DMD) is an inherited disease characterized by early onset of skeletal muscle degeneration and progressive weakness. Although dilated cardiomyopathy may occur during adolescence, it is often undetected early in its course because of physical inactivity and generalized debilitation. The purpose of this study was to apply the technique of cardiac magnetic resonance (CMR) tagging to detect occult cardiac dysfunction in young subjects with DMD by measuring myocardial strain and torsion. Methods and Results-Thirteen DMD pediatric subjects without clinically apparent heart disease and 9 age-matched healthy males were recruited. Each was scanned on a 1.5-T clinical scanner to acquire contiguous short-axis planes from the apex to the mitral valve plane and then 3 tagged images at base, midventricle, and apex. Global and segmental myocardial net twist and circumferential strain were computed with the use of 2D homogeneous strain analysis. Ventricular torsion was computed by normalizing net twist by the distance from apex to mitral valve plane. DMD patients exhibited normal left ventricular volumes and ejection fractions but manifested reduced midventricular and basal cross-sectional global circumferential strain compared with the reference group (PϽ0.005). These alterations also appeared in segmental analyses in the septal, anterior, lateral, and inferior walls (PϽ0.05). Conclusions-In patients predisposed to cardiomyopathies because of dystrophinopathy, occult regional cardiac dysfunction can be diagnosed with CMR tagging. This method of strain imaging analysis may offer a sensitive approach for delineating the presence and progression of cardiovascular disease and for assessing therapies designed to modulate the onset and course of heart failure.

T-cell activation up-regulates CD30 resulting in an increase in serum soluble CD30 (sCD30). CD4+ T cells, a major source for sCD30, play a significant role in the pathogenesis of rejection. In this study, sCD30 was measured pre-and posttransplant in mouse islet allograft models and human islet allograft recipients. sCD30 was measured by ELISA in diabetic C57BL/6, CD4Knockout (KO) and CD8KO islet allograft recipients. sCD30 increased significantly prior to rejection (1.8 ± 1 days) in 80% of allograft recipients. Sensitization with donor splenocytes, or a second graft, further increased sCD30 (282.5 ± 53.5 for the rejecting first graft vs. 374.6 ± 129 for the rejecting second graft) prior to rejection suggesting memory CD4+ T cells contribute to sCD30. CD4KO failed to reject islet allograft and did not demonstrate sCD30 increase. CD8KO showed elevated (227 ± 107) sCD30 (1 day) prior to rejection. High pretransplant sCD30 (>20 U/ml) correlated with poor outcome in human islet allograft recipients. Further, increase in sCD30 posttransplant preceded (3-4 months) loss of islet function. We conclude that sCD30 is released from activated CD4 T cells prior to islet allograft rejection and monitoring sCD30 can be a valuable adjunct in the follow-up of islet transplant recipients.

In the mustached bat, the primary auditory cortex (AI) can be divided into three subdivisions: the Doppler-shifted constant-frequency processing (DSCF) area, and the anterior (AIa) and posterior (AIp) regions. The DSCF area is composed of two subdivisions: excitatory-excitatory (E-E) and inhibitory-excitatory (I-E). The E-E division is located in the ventral portion of the DSCF area and mainly consists of neurons excited bilaterally, while the I-E division is located in the dorsal portion and mainly consists of neurons which are inhibited by ipsilateral ear stimuli, but excited by contralateral ear stimuli. The E-E division is bilaterally connected by commissural fibers, while the I-E division is not. The AIa and AIp regions have neither E-E neurons nor commissural connections. In the AI of the cat, E-E and I-E neurons form alternating bands which are parallel to the frequency axis. E-E bands are bilaterally connected by commissural fibers, but I-E bands are not. The DSCF area shares a similar functional organization with the AI of the cat.

had cirrhosis with Child-Pugh score <8. The prescribed dose was 40 Gy in four fractions. Dose reduction was permitted for normal organ dose constrains. The bile duct (BD) was delineated from the common bile duct to the first bifurcation of left and right intrahepatic duct. In addition, the central hepatobiliary tract (cHBT) was defined by a 10 or 15 mm expansion of the portal vein from the splenic confluence to the first bifurcation of left and right portal veins. We analyzed the clinical and dosimetric parameters, including multiple dose-volume histogram endpoints: D max (the maximum point dose), D mean (the mean dose), V 40Gy (volume of cHBT that received 40 Gy), V 37Gy , V 34Gy. Receiver operator curves (ROC) defined optimal dosimetric thresholds for analysis. HB toxicities were graded according to Common Terminology Criteria for Adverse Events version 4.0 and we defined grade 3+ HB toxicity as a severe HB toxicity. Results: Median follow-up duration was 9.9 months after SABR. Eight out of 28 patients (28.6%) experienced severe HB toxicity. Among clinical and dosimetric parameters, V 40Gy of cHBT with 10 mm expansion were highly associated with severe HB toxicity: V 40Gy >40 cm 3 (relative risk [RR] Z 3.2, P < 0.011). However, clinical or other dosimetric factors, D max or D mean of BD and cHBT, did not have predictive value. The risk of severe HB toxicity for V 40Gy 20 cm 3 , > 20 cm 3 , > 30 cm 3 , and > 40 cm 3 are 8.3% (n Z 1/12), 41.2% (n Z 7/17), 46.2% (n Z 6/13), and 54.5% (n Z 6/11), respectively. Conclusion: SABR to the central liver lesions should be used with caution due to the risk of HB toxicity. Radiation doses to cHBT are associated with development of severe HB toxicity. We suggest that V 40Gy <20 cm 3 as a potential dose constraint for cHBT when delivered in four fractions.

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