4-Levels Vertically Stacked SiGe Channel Nanowires Gate-All-Around Transistor with Novel Channel Releasing and Source and Drain Silicide Process.

In this paper, the fabrication and electrical performance optimization of a four-levels vertically stacked Si0.7Ge0.3 channel nanowires gate-all-around transistor are explored in detail. First, a high crystalline quality and uniform stacked Si0.7Ge0.3/Si film is achieved by optimizing the epitaxial growth process and a vertical profile of stacked Si0.7Ge0.3/Si fin is attained by further optimizing the etching process under the HBr/He/O2 plasma. Moreover, a novel ACT@SG-201 solution without any dilution at the temperature of 40 °C is chosen as the optimal etching solution for the release process of Si0.7Ge0.3 channel. As a result, the selectivity of Si to Si0.7Ge0.3 can reach 32.84 with a signature of "rectangular" Si0.7Ge0.3 extremities after channel release. Based on these newly developed processes, a 4-levels vertically stacked Si0.7Ge0.3 nanowires gate-all-around device is prepared successfully. An excellent subthreshold slope of 77 mV/dec, drain induced barrier-lowering of 19 mV/V, Ion/Ioff ratio of 9 × 105 and maximum of transconductance of ~83.35 µS/µm are demonstrated. However, its driven current is only ~38.6 µA/µm under VDS = VGS = -0.8 V due to its large resistance of source and drain (9.2 × 105 Ω). Therefore, a source and drain silicide process is implemented and its driven current can increase to 258.6 µA/µm (about 6.7 times) due to the decrease of resistance of source and drain to 6.4 × 104 Ω. Meanwhile, it is found that a slight increase of leakage after the silicide process online results in a slight deterioration of the subthreshold slope and Ion/Ioff ratio. Its leakage performance needs to be further improved through the co-optimization of source and drain implantation and silicide process in the future.

Protective effect of caffeic acid phenethyl ester against imidacloprid-induced hepatotoxicity by attenuating oxidative stress, endoplasmic reticulum stress, inflammation and apoptosis.

Imidacloprid (IMI) is a widely used neonicotinoid pesticide in the world, its environmental and human health risk has particularly attracted the attention of researchers. Caffeic acid phenethyl ester (CAPE), an active polyphenol of propolis, has many pharmacological activities including free radical scavenger, anti-inflammatory, and anti-oxidant. In this study, protective effect of CAPE against IMI induced liver injury in mice was performed. Administration of 1 and 2.5 mg/kg CAPE markedly prevented serum AST and ALT increase in 5 mg/kg IMI-induced mice. CAPE significantly downregulated liver NO generation and lipid peroxidation, and upregulated glutathione, catalase, superoxide dismutase and glutathione peroxidase in a dose-dependent manner in liver of IMI-induced mice. Endoplasmic reticulum stress represented by the swelling of endoplasmic reticulum was observed by transmission electron microscope in IMI group. Pretreatment of 2.5 mg/kg CAPE significantly attenuated the endoplasmic reticulum stress induced by IMI in liver. Western blot analysis illustrated that pretreatment of CAPE downregulated the upregulation of TNF-α and IFN-γ induced by IMI in liver of mice. Moreover, the increase of positive apoptotic hepatocytes further suggested apoptosis might be involved in IMI-induced hepatotoxicity. Pretreatment of 1 and 2.5 mg/kg CAPE significantly decreased positive apoptotic hepatocytes, suggested that CAPE prevented apoptosis in liver of IMI-induced mice. In conclusion, CAPE prevented liver injury in IMI-induced mice via attenuation of oxidative stress, endoplasmic reticulum stress, inflammation and apoptosis. Our findings may have broad biological and environmental implications for future research on the therapeutic strategy to prevent liver injury induced by pesticides.

Mipu1, a novel direct target gene, is involved in hypoxia inducible factor 1-mediated cytoprotection.

Mipu1 (myocardial ischemic preconditioning up-regulated protein 1), recently identified in our lab, is a novel zinc-finger transcription factor which is up-regulated during ischemic preconditioning. However, it is not clear what transcription factor contributes to its inducible expression. In the present study, we reported that HIF-1 regulates the inducible expression of Mipu1 which is involved in the cytoprotection of HIF-1α against oxidative stress by inhibiting Bax expression. Our results showed that the inducible expression of Mipu1 was associated with the expression and activation of transcription factor HIF-1 as indicated by cobalt chloride (CoCl2) treatment, HIF-1α overexpression and knockdown assays. EMSA and luciferase reporter gene assays showed that HIF-1α bound to the hypoxia response element (HRE) within Mipu1 promoter region and promoted its transcription. Moreover, our results revealed that Mipu1 inhibited the expression of Bax, an important pro-apoptosis protein associated with the intrinsic pathway of apoptosis, elevating the cytoprotection of HIF-1 against hydrogen peroxide (H2O2)-mediated injury in H9C2 cells. Our findings implied that Bax may be a potential target gene of transcription factor Mipu1, and provided a novel insight for understanding the cytoprotection of HIF-1 and new clues for further elucidating the mechanisms by which Mipu1 protects cell against pathological stress.