The comparison of gamma-radiation and electrical stress influences on oxide and interface defects in power VDMOSFET

The behaviour of oxide and interface defects in n-channel power vertical double-diffused metal-oxide-semiconductor field-effect transistors, firstly degraded by the gamma-irradiation and electric field and subsequently recovered and annealed, is presented. By analyzing the transfer characteristic shifts, the changes of threshold voltage and underlying changes of gate oxide and interface trap densities during the stress (recovery, annealing) of investigated devices, it is shown that these two types of stress influence differently on the gate oxide and the SiO2-Si interface. [Projekat Ministarstva nauke Republike Srbije, br. OI171026

Annealing of radiation-induced defects in burn-in stressed power VDMOSFETs

The annealing of radiation-induced defects in burn-in stressed n-channel power VDMOSFETs with thick gate oxides (100 and 120 nm) is analysed. In comparison with the previous spontaneous recovery, the changes of device electrical parameters observed during annealing are highlighted by the elevated temperature and voltage applied to the gate, and are more pronounced in devices with a 120 nm thick gate oxide. The threshold voltage of VDMOSFETs with a 100 nm thick gate oxide during annealing has an initially slow growth, but then increases rapidly and reaches the value higher than the pre-irradiation one (rebound effect). In the case of devices with a 120 nm thick gate oxide, the threshold voltage behaviour also consists of a slight initial increase followed by a rapid, but dilatory increase, with an obvious tendency to achieve the rebound. The changes of channel carrier mobility during annealing are similar in all samples: at first, it slowly and then rapidly declines, and after reaching the minimum it begins to increase. In the case of VDMOSFETs with a thicker gate oxide, these changes are much slower. The underlying changes in the densities of gate oxide-trapped charge and interface traps are also delayed in devices with a thicker gate oxide. All these phenomena occur with certain delay in burn-in stressed devices compared to unstressed ones. The leading role in the mechanisms responsible for the observed phenomena is attributed to hydrogen related species

NBTI and irradiation related degradation mechanisms in power VDMOS transistors

In this paper it is shown that NBT stress effects in previously irradiated devices are strongly dependent on the total dose received. Namely, in the case of low-dose irradiation the subsequent NBT stress seems to lead to further device degradation. On the other hand, in the case of devices previously irradiated to higher doses, NBT stress seems to have positive role as it practically anneals a part of radiation-induced degradation. The total dose received at which NBT stress almost completely anneals radiation-induced degradation is determined to be around 60 Gy

Effects in Commercial p-Channel Power VDMOS Transistors Initiated by Negative Bias Temperature Stress and Irradiation

This paper investigates the impact of negative bias temperature stress on irradiated commercial p-channel power VDMOS transistors, particularly focusing on gate oxide charge and interface trap alterations and their contribution to threshold voltage shifts. The study addresses the critical issue of transistor reliability, as threshold voltage shifts can significantly affect device performance, especially in elevated temperature and negative gate oxide field conditions. Additionally, the research explores the effects of irradiation on VDMOS power transistors, emphasizing the importance of understanding the associated electrical parameter changes. The paper presents a comprehensive analysis of static and pulsed NBT stressing, with a specific focus on novel stress signals encountered in practical applications. The experimental procedure involves irradiation and NBT stress, and the results reveal insights into the contributions of gate oxide charge and interface traps to threshold voltage shifts. The findings shed light on the reliability of electronic equipment incorporating p-channel power VDMOS transistors under various stress conditions, offering valuable insights for device design and operation.MIEL : 33nd International Conference on Microelectronics; October 16-18, 2023, Niš, SerbiaIEEE Catalog No. CFP23432-US

Characterization of thymocyte phenotypic alterations induced by long-lasting beta-adrenoceptor blockade in vivo and its effects on thymocyte proliferation and apoptosis

Adult male Wistar rats were subjected to propranolol (P, 0.40 mg/100 g/day) or saline (S) administration (controls) over 14 days. The expression of major differentiation molecules on thymocytes and Thy-1 (CD90) molecules, which are shown to adjust thymocyte sensitivity to TCR alpha beta signaling, was studied. In addition, the sensitivity of thymocytes to induction of apoptosis and concanavalin A (Con A) signaling was estimated. The thymocytes from P-treated (PT) rats exhibited an increased sensitivity to induction of apoptosis, as well as to Con A stimulation. Furthermore, P treatment produced changes in the distribution of thymocyte subsets suggesting that more cells passed positive selection and further differentiated into mature CD4+ or CD8+ single positive (SP) TCR alpha beta(high) cells. These changes may, at least partly, be related to the markedly increased density of Thy-1 surface expression on TCR alpha beta(low) thymocytes from these rats. The increased frequency of cells expressing the CD4+25+ phenotype, which has been shown to be characteristic for regulatory cells in the thymus, may also indicate alterations in thymocyte selection following P treatment. Inasmuch as positive and negative selections play an important role in continuously reshaping the T-cell repertoire and maintaining tolerance, the hereby presented study suggests that pharmacological manipulations with beta-AR signaling, or chemically evoked alterations in catecholamine release, may interfere with the regulation of thymocyte selection, and consequently with the immune response