The characteristics and outcome in 10 patients who underwent retransplantation after losing their renal grafts to BK virus-associated nephropathy (BKAN) are described. The patients underwent retransplantation at a mean of 13.3 months after failure of the first graft. Nephroureterectomy of the first graft was performed in seven patients. Maintenance immunosuppression regimens after the first and second grafts were similar, consisting of a combination of a calcineurin inhibitor, mycophenolate mofetil, and prednisone. BKAN recurred in one patient 8 months after retransplantation, but stabilization of graft function was achieved with a decrease in immunosuppression and treatment with low-dose cidofovir. After a mean follow-up of 34.6 months, all patients were found to have good graft function with a mean creatinine of 1.5 mg/dL. From this collective experience from five transplant centers (although the follow-up after retransplantation was not extensive), it can be concluded that patients with graft loss caused by BKAN can safely undergo retransplantation. The risk of recurrence does not seem to be increased in comparison with the first graft.

Interruption of the renin-angiotensin-aldosterone system (RAAS) at different levels is target-organ protective in several disease states; however, complete blockade is unlikely to be achieved due to escape mechanisms whenever blockade is attempted, incomplete knowledge of the role of all elements of the RAAS, and lack of pharmacotherapy against some elements that have been shown to contribute to disease states. Aldosterone has been overlooked as a mediator of RAAS escape and a key factor in target-organ injury despite the use of available RAAS blockers. Aldosterone is thought to play a role in the development of hypertension, alteration in vascular structure, vascular smooth muscle hypertrophy, endothelial dysfunction, structural renal injury, proteinuria, left ventricular remodeling, collagen synthesis, and myocardial fibrosis. Aldosterone receptor antagonists have been shown to antagonize all these effects in experimental models. Clinical trials with aldosterone antagonists showed an improvement in survival and left ventricular mass index in patients with congestive heart failure, and a reduction in urinary protein excretion and left ventricular mass index in patients with type 2 diabetes and early nephropathy who developed aldosterone synthesis escape. Consequently, aldosterone receptor antagonists may have specific benefits for reducing target-organ injury, particularly if there is evidence of RAAS escape.

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In this paper, bottom-oxide thickness (T bo ) and program/erase stress effects on charge retention in SONOS Flash memory cells with FN programming are investigated. Utilizing a numerical analysis based on a multiple electron-trapping model to solve the Shockley-Read-Hall rate equations in nitride, we simulate the electron-retention behavior in a SONOS cell with T bo from 1.8 to 5.0 nm. In our model, the nitride traps have a continuous energy distribution. A series of Frenkel-Poole (FP) excitation of trapped electrons to the conduction band and electron recapture into nitride traps feature the transitions between the conduction band and trap states. Conduction band electron tunneling via oxide traps created by high-voltage stress and trapped electron direct tunneling through the bottom oxide are included to describe various charge leakage paths. We measure the nitride-charge leakage current directly in a large-area device for comparison. This paper reveals that the charge-retention loss in a high-voltage stressed cell, with a thicker bottom oxide (5 nm), exhibits two stages. The charge-leakage current is limited by oxide trap-assisted tunneling in the first stage and, then, follows a 1/t time dependence due to the FP emission in the second stage. The transition time from the first stage to the second stage is related to oxide trap-assisted tunneling time but is prolonged by a factor. Index Terms-Oxide thickness, positive oxide charge-assisted tunneling, Shockley-Read-Hall (SRH) rate equation, SONOS retention mechanisms.

We investigate the characteristic deformation behavior of rubber with carbon black (CB) filler. The deformation behaviors of a plane strain rubber unit cell containing CB fillers under monotonic and cyclic strain are investigated by computational simulation with a nonaffine molecular-chain network model. The results reveal the substantial enhancement of the resistance of the rubber to macroscopic deformation, which is caused by the marked orientation hardening due to the highly localized deformation in the rubber. The disentanglement of the molecular chain during the deformation of rubber results in the magnification of the hysteresis loss, i.e., the Mullins effect, occurring in stress-stretch curves under cyclic deformation processes. The increase in volume fraction and in aggregation of the distribution of CB substantially raises the resistance of the rubber to deformation and hysteresis loss. The effect of the heterogeneous distribution of the initial average number of segments of molecular chains on the hysteresis loss has been clarified. r