The existence of quantum confinement effects in nanoscaled conduction channels results in which the behaviors of electrons and phonons will become drastically different from those in bulk materials. This is especially true in the junction regions

where the nanochannel is linked with the electronic and thermal reservoirs. The present study investigated the structural effect of pyramidal and abrupt junctions in heat exchange between electron and phonon subsystems in the transport through a quantum dot (QD). The numerical results indicated that by confining the electronic and phononic wave functions C59 price in the pyramidal junctions, a higher saturation heat exchange would be reached at a lower bias, compared to that of the abrupt junction. The pyramidal junction also becomes more subjected to size effects, where the saturation heat exchange

decreases as the size of the junction increases. Such an effect is less significant in the abrupt junctions. Surface reconstruction induced bond stiffening in the pyramidal junctions plays a dominant role in modulating the junction heat exchange by blockading the phonon Selleckchem ZD1839 transportation between the reservoirs through the QD, which effectively reducing the amount of heat being generated. The results may provide new insights on the fundamental science and relationship between contact atomic structures and thermal dissipations in nanoelectronics. (C) 2010 American Institute of Physics. [doi:10.1063/1.3437650]“
“We describe the decline in islet function, in relation to HLA sensitization, in an islet transplant recipient and the recovery of this function after treatment with DMH1 anti-CD20 monoclonal antibody and IV immunoglobulins. A 51-year-old woman with type 1 diabetes received one intraportal islet infusion. Following this transplantation,

she became insulin independent. A search for HLA antibodies by using an ELISA technique remained consistently negative for HLA class I and II. It was only 2 years after the islet transplantation that this search became positive against class II antigens, reaching a peak of reactivity concomitantly with the appearance of a deterioration of glucose control requiring low-dose insulin therapy. Luminex((R)) screening and single-antigen assays then revealed the presence of both nondonor-specific and donor-specific antibodies against HLA class II molecules. This immunization, already present in the pretransplant serum, had increased during the 6 months preceding the clinical deterioration. Since these data nevertheless pointed to antibody-mediated rejection of the islet allograft, treatment with anti-CD20 monoclonal antibody and IV immunoglobulins was initiated. One month later, the search by ELISA for antibodies against HLA class II antigens became negative, the Luminex((R)) tests normalizing more gradually.