Modeling of the hot electron subpopulation and its application toimpact ionization in submicron silicon devices-Part II: numericalsolutions

A macroscopic transport model for the hot electron subpopulation (HES) and a nonlocal impact ionization (II) model were proposed in Part I of this article: see ibid. p. 1200, 1994. The transport equations have been derived from the Boltzmann transport equation (BTE) and closure has been provided by an empirically determined equation. The transport equations and the II model have been calibrated using data obtained from self-consistent Monte Carlo (SCMC) simulations. In this article we present the numerical solutions obtained by applying the proposed model to n⁺- n^--n⁺ structures with various doping profiles. The results are compared to the data obtained from SCMC simulations and also to those obtained from models proposed earlier by other authors     

Modeling of the hot electron subpopulation and its application toimpact ionization in submicron silicon devices-Part I: transportequations

Impact ionization (II) in three different n⁺-n^- -n⁺ device structures is investigated using self-consistent Monte Carlo simulations. A subset of electrons participating in II-referred to as the hot electron subpopulation (HES)-is identified. The data obtained from the Monte Carlo (MC) simulations indicate that the average energy of the HES (ω˜) is an appropriate variable for the macroscopic quantification of II in all the devices under consideration. In order to calculate ω˜, a set of macroscopic transport equations for the HES is derived from the Boltzmann transport equation and calibrated using data from the MC simulations. Numerical solutions to the proposed II model applied to the three devices considered here will be presented in Part II. Therein, values of the II coefficient (IIC) predicted by our model will be compared to those obtained from our MC simulations and also to IIC values predicted by models proposed earlier by other authors     

Aplastic anaemia and paroxysmal nocturnal haemoglobinuria: a study of the GPI-anchored proteins on human platelets

Twenty-six consecutive patients with acquired aplastic anaemia (AA) and nine patients with de novo paroxysmal nocturnal haemoglobinuria (PNH) were included in this study. In these 35 patients a GPI-anchored molecule defect at the platelet surface was investigated by flow-cytometry. Platelets from eight out of the nine patients with de novo PNH were found to be deficient for the GPI-anchored molecule CD55, CD58 and CD59. We also detected a GPI-anchored molecule defect on monocytes, granulocytes, and erythrocytes in all patients with de novo PNH. Among the 26 AA patients, a GPI defect was detected on platelets in five patients. Interestingly, these five patients were also found to have a GPI-anchored molecule defect on erythrocytes, whereas in 10 patients the GPI-anchored molecule defect was only detected on monocyte and polymorphonuclear (PMN) cells.