Mechanism analysis of gate-induced drain leakage in off-state n-MOSFET

An analytical expression for both band-to-band and band-trap-band indirect tunnelings is used to study the gate-induced drain leakage (GIDL) current of MOSFETs measured before and after hot-carrier stress. The voltage and temperature dependence of GIDL are characterized. Both results show that interface traps situated near the midgap participate in the conduction of GIDL, and band-trap-band indirect tunneling could be the major mechanism. This is further supported by the fact that the percentage increase in GIDL induced by hot-carrier stress is about the same as the corresponding increase in interface-trap density. On the other hand, under low-field conditions, trap-assisted Poole–Frenkle emission dominates over tunneling for temperatures even well below room temperature.     

Effects of thymectomy and glucocorticoid therapy on peripheral lymphocytes in myasthenia gravis

Clinical manifestations and peripheral blood lymphocyte subset changes were studied in patients with myasthenia gravis (MG) to elucidate the mechanism of clinical improvement following treatment, with thymectomy (Tx) or glucocorticoid (GC) therapy. The changes found were: 1. There was a significant increase in percentages of CD3+, CD29+ CD4+ cells and CD4/CD8 ratio and a significant decrease in percentages of CD8+ and CD16,56+ cells in patients who had never been treated with any immune therapy. 2. After Tx or GC therapy, CD3+ and CD4+, CD29+ cells were decreased, but the number CD19+ and CD16, CD56 cells did not change. 3. Tx had a special effect on CD8+ cells. In most of the patients who showed clinical improvement after Tx, CD8+ cells were increased and CD4/CD8 ratio wad decreased. 4. Anti-acetylcholine receptor (AChRAb) titers were markedly decreased after GC therapy. These results indicate that there were obvious abnormalities in cell-mediated immunity in addition to those in humoral immunity in myasthenia gravis. These abnormalities tended to be normalized after Tx or GC therapy.     

Kinetics of modification of the mitochondrial succinate-ubiquinone reductase by 5,5''-dithiobis-(2-nitro-benzoic acid)

In the present study, we examined the effect of the thromboxane/prostaglandin endoperoxide analogue U46619 on proliferation and hypertrophy in cultured rat vascular smooth muscle cells and the roles of protein kinase C and transforming growth factor-beta (TGF-beta) in the mediation of the hypertrophic response to U46619. Since an increase in basic fibroblast growth factor (bFGF) was previously shown to mediate the hypertrophic response to U46619, we also assessed the relationship between bFGF and TGF-beta in the expression of U46619 actions. U46619 increased [35S]methionine incorporation into protein and protein content of vascular smooth muscle cells but had no effect on cell number. A role for TGF-beta was supported by the following observations: (1) exogenous human TGF-beta 1 increased protein synthesis; (2) antibody to TGF-beta blocked both TGF-beta- and U46619-induced increases in protein content; (3) U46619 increased active and total TGF-beta bioactivities; and (4) the actions of U46619 on protein content and TGF-beta bioactivity were blocked by the thromboxane/prostaglandin endoperoxide receptor antagonist SQ 29,548. Previous observations had demonstrated a role for bFGF in the expression of U46619 actions on protein synthesis. Results of the present study suggest that TGF-beta and bFGF interact in mediating the protein synthetic response to U46619. First, the concentration of exogenous TGF-beta (10 pmol/L) alone required to produce a protein synthetic response equivalent to that induced by U46619 was much higher than the concentration of endogenous active TGF-beta that accumulated in the media in response to U46619 (0.7 pmol/L). Second, bFGF (20 ng/mL) increased total TGF-beta bioactivity and stimulated protein synthesis. The hyper-trophic response to bFGF was blocked by anti-TGF-beta. The ability of U46619 and bFGF to increase protein synthesis and protein content in vascular smooth muscle cells was associated with TGF-beta-induced suppression of proliferation, as evidenced by the ability of antibody to TGF-beta to enhance U46619- and bFGF-induced increases in [3H]thymidine incorporation into DNA. Results of the present study also supported a role for protein kinase C in the expression of U46619 and bFGF actions. U46619 increased protein kinase C activity in the particulate fraction of vascular smooth muscle cells. Moreover, the protein kinase C inhibitors GF109203X and staurosporine blocked U46619- and bFGF-induced increases in protein synthesis as well as active and total TGF-beta bioactivities. By contrast, the protein kinase C inhibitors did not prevent the increases in protein synthesis induced by exogenous TGF-beta. The results demonstrate that thromboxane/prostaglandin endoperoxide signals increased TGF-beta bioactivity via protein kinase C. Increases in both bFGF and TGF-beta are required for an optimal hypertrophic response to U46619. The hypertrophic response to TGF-beta occurs through a protein kinase C-independent pathway.     

^125I,^131I诱发小鼠精子畸形发生率比较

本文选用 ICR 雄性小鼠,经腹腔分别注射不同剂量的~(125)I 及~(131)I,观察并比较它们对小鼠精子畸形发生率的影响及染毒后睾丸中放射性活度的变化。实验结果表明:(1)~(125)I 染毒后4—5周,0、185、370和555 kBq 各组精子畸形发生率分别为9.00‰、9.57‰、11.6‰及13.9‰;~(131)I 染毒后4—5周,上述各组精子畸形发生率分别为8.50‰、12.5‰、14.7‰和15.5‰;在相同注入量下,~(125)I 与~(131)I 诱发小鼠精子畸形发生率的差异各组均不显著(X~2检验,p>0.05)。(2)~(125)I、~(131)I 染毒后2h 至7天内,两者在睾丸中的放射性活度及变化规律相似,即在染毒后2h 达最高值,每克睾丸中~(125)I 和~(131)I 的放射性活度分别占初始注入量(370 kBq)的0.72％和0.50％,然后迅速下降,至一周时,仅分别占初始注入量的0.035％和0.011％。     

剂量率对聚四氟乙烯辐射裂解的影响

本文研究了在以电子加速器的电子射线为辐射源时,剂量率对PTFE辐射裂解的影响。在剂量相同的条件下,剂量率从1.44×10~4 rad/s增至5.75×10~4 rad/s,裂解效率提高3.3倍。剂量率和各断裂参数(单位剂量裂解度a_0,G(s)值等)均成线性关系。当裂解度一定时,剂量率与剂量成反变关系。     

Delphi开发环境下的实时数据采集程序设计

本文介绍了利用Delphi开发平台开发数据采集程序的两种方法，并结合某测深仪给出了一个编程的例子.     

Fabrication of optical fibre nanowires and their optical and mechanical characterisation

It is demonstrated for the first time that long nanowires with radii as small as 30 nm can be manufactured with a conventional coupler fabrication rig. The temporal deterioration of nanowire optical properties has been studied and correlated with its mechanical behaviour. The original transmission properties have been restored by a post-fabrication treatment.