6 research outputs found

    Embedded DRAM using c-axis-aligned crystalline In-Ga-Zn oxide FET with 1.8V-power-supply voltage

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    An embedded memory using c-axis aligned crystalline In-Ga-Zn oxide (CAAC-IGZO) FETs with an extremely low off-state current on the order of yoctoamperes (yA) (yocto- is a metric prefix denoting a factor of 10-24) is known as a potential next-generation memory [1][2]. A dynamic oxide semiconductor RAM (DOSRAM), where each memory cell is composed of one CAAC-IGZO FET and one capacitor, enables long data retention and long interval of refresh operations with an advantage of extremely low off-state current of the CAAC-IGZO FET. However, negative backgate voltage (Vbg) and word-line driving voltages of 0/3.3 V (VSSL/VDDH) had been required for an access transistor of the memory cell to satisfy high on-state current and low off-state current. This work shows that DOSRAM operates with 1.8 V-power supply voltage by using a novel driving method. Figure 1 shows Vg-Id performance of a CAAC-IGZO FET used as a cell transistor. The threshold voltage (Vth) of the CAAC-IGZO FET is controlled by changing a level of Vbg, whereas Vth of the Si FET is controlled by channel doping. Figure 2 shows a block diagram of a prototyped DOSRAM. The refresh rate in DOSRAM mainly depends on the leakage current of cell transistors. To reduce the refresh rate to once an hour, the off-state current of the cell transistors on a non-selected word line needs to be reduced to 200 zeptoamperes (zA) per FET (zepto- is a metric prefix denoting a factor of 10-21) or lower at 85C. The required Vbg is -7.0 V to achieve such an off-state current at Vg 0 V, for example. To obtain approx. 100 MHz-driving frequency, the required on-state current is at least several microamperes. The voltage level difference in the word line, VDDH VSSL, is a factor that determines the on-state current, and in this work is fixed to 3.3 V so that the combination of Vbg and the word line voltage is optimized. The application of negative voltage to the word line enables the leakage current of the cell transistor to be maintained low even when Vbg is increased. For example, whereas the existing driving method meets the above off-state current value with Vbg -7.0 V and the VSSL 0 V, the novel driving method meets the value with Vbg 0 V and VSSL -1.5 V. In the novel driving method, VDDH 1.8 V. There has been a report of a reduction in leakage current of a memory cell by application of negative voltage to a top gate in DRAM using Si CMOS [3]. In contrast to it, DOSRAM including CAAC-IGZO FETs with L 60 nm has a leakage current of 200 zA or lower, which is 7-digit lower than that of the DRAM using Si CMOS, and enables longer data retention. The evaluation results of the prototyped DOSRAM verify that a reduction in power-supply voltage from 3.3 V to 1.8 V is possible in terms of operation and data retention. This suggests a highly compatible and efficient configuration of an embedded DRAM and a logic circuit where signals can be transmitted with low VDD. References [1] S. H. Wu, et al., IEEE Symp. VLSI Tech., pp. 166-167, 2017. [2] T. Ishizu, et al., IEEE Symp. VLSI Cir., pp. 162-163, 2017. [3] F. Hamzaoglu et al., IEEE Journal of Solid-State Circuits, vol. 50, no. 1, pp. 150-157, Jan. 2015

    Effectiveness of <italic>c</italic>-Axis Aligned Crystalline IGZO FET as Selector Element and Ferroelectric Capacitor Scaling of 1T1C FeRAM

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    Aiming to reduce the area of a ferroelectric random access memory (FeRAM), we fabricated an FeRAM having a 1T1C configuration by using a c{c} -axis aligned crystalline In-Ga-Zn-O field-effect transistor, which we call OSFET, with a high breakdown voltage. A combination of the OSFET with L/W{L}/{W} of 60 nm/60 nm and a single damascene ferroelectric capacitor (FE-Cap) attained FE-Cap area reduction to 0.06 μm 20.06~\mu \text{m}~^{\mathrm{ 2}} per cell. The FeRAM achieved a write time of 10 ns, a rewriting endurance of 109 cycles, and a data retention time of 100 min at 85&#x00B0;C. The OSFET is an optimal selector element for emerging memories

    A small molecule iCDM-34 identified by in silico screening suppresses HBV DNA through activation of aryl hydrocarbon receptor

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    Abstract IFN-alpha have been reported to suppress hepatitis B virus (HBV) cccDNA via APOBEC3 cytidine deaminase activity through interferon signaling. To develop a novel anti-HBV drug for a functional cure, we performed in silico screening of the binding compounds fitting the steric structure of the IFN-alpha-binding pocket in IFNAR2. We identified 37 compounds and named them in silico cccDNA modulator (iCDM)-1–37. We found that iCDM-34, a new small molecule with a pyrazole moiety, showed anti-HCV and anti-HBV activities. We measured the anti-HBV activity of iCDM-34 dependent on or independent of entecavir (ETV). iCDM-34 suppressed HBV DNA, pgRNA, HBsAg, and HBeAg, and also clearly exhibited additive inhibitory effects on the suppression of HBV DNA with ETV. We confirmed metabolic stability of iCDM-34 was stable in human liver microsomal fraction. Furthermore, anti-HBV activity in human hepatocyte-chimeric mice revealed that iCDM-34 was not effective as a single reagent, but when combined with ETV, it suppressed HBV DNA compared to ETV alone. Phosphoproteome and Western blotting analysis showed that iCDM-34 did not activate IFN-signaling. The transcriptome analysis of interferon-stimulated genes revealed no increase in expression, whereas downstream factors of aryl hydrocarbon receptor (AhR) showed increased levels of the expression. CDK1/2 and phospho-SAMHD1 levels decreased under iCDM-34 treatment. In addition, AhR knockdown inhibited anti-HCV activity of iCDM-34 in HCV replicon cells. These results suggest that iCDM-34 decreases the phosphorylation of SAMHD1 through CDK1/2, and suppresses HCV replicon RNA, HBV DNA, and pgRNA formation

    First evidence of tick-borne encephalitis (TBE) outside of Hokkaido Island in Japan

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    ABSTRACTTick-borne encephalitis (TBE) is an infection of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is endemic in parts of Europe and Asia. TBEV is transmitted to humans primarily by Ixodes ticks. There have been 5 TBE cases identified in Japan, all on the northern island of Hokkaido. Rodents with TBEV antibodies and Ixodes ticks have been identified throughout Japan, indicating that TBEV infection might be undiagnosed in Japan. Residual serum and cerebrospinal fluid (CSF) collected in 2010–2021 from 520 patients ≥1 year-of-age previously hospitalized with encephalitis or meningitis of unknown etiology at 15 hospitals (including 13 hospitals outside of Hokkaido) were screened by ELISA for TBEV IgG and IgM antibodies; TBEV infection was confirmed by the gold standard neutralization test. Residual serum was available from 331 (63.6%) patients and CSF from 430 (82.6%) patients; both serum and CSF were available from 189 (36.3%). Two patients were TBE cases: a female aged 61 years hospitalized for 104 days in Oita (2000 km south of Hokkaido) and a male aged 24 years hospitalized for 11 days in Tokyo (1200 km south of Hokkaido). Retrospective testing also identified a previous TBEV infection in a female aged 45 years hospitalized for 12 days in Okayama (1700 km south of Hokkaido). TBEV infection should be considered as a potential cause of encephalitis or meningitis in Japan. TBE cases are likely undiagnosed in Japan, including outside of Hokkaido, due to limited clinical awareness and lack of availability of TBE diagnostic tests

    A small molecule iCDM-34 identified by in silico screening suppresses HBV DNA through activation of aryl hydrocarbon receptor

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    IFN-alpha have been reported to suppress hepatitis B virus (HBV) cccDNA via APOBEC3 cytidine deaminase activity through interferon signaling. To develop a novel anti-HBV drug for a functional cure, we performed in silico screening of the binding compounds fitting the steric structure of the IFN-alpha-binding pocket in IFNAR2. We identified 37 compounds and named them in silico cccDNA modulator (iCDM)-1–37. We found that iCDM-34, a new small molecule with a pyrazole moiety, showed anti-HCV and anti-HBV activities. We measured the anti-HBV activity of iCDM-34 dependent on or independent of entecavir (ETV). iCDM-34 suppressed HBV DNA, pgRNA, HBsAg, and HBeAg, and also clearly exhibited additive inhibitory effects on the suppression of HBV DNA with ETV. We confirmed metabolic stability of iCDM-34 was stable in human liver microsomal fraction. Furthermore, anti-HBV activity in human hepatocyte-chimeric mice revealed that iCDM-34 was not effective as a single reagent, but when combined with ETV, it suppressed HBV DNA compared to ETV alone. Phosphoproteome and Western blotting analysis showed that iCDM-34 did not activate IFN-signaling. The transcriptome analysis of interferon-stimulated genes revealed no increase in expression, whereas downstream factors of aryl hydrocarbon receptor (AhR) showed increased levels of the expression. CDK1/2 and phospho-SAMHD1 levels decreased under iCDM-34 treatment. In addition, AhR knockdown inhibited anti-HCV activity of iCDM-34 in HCV replicon cells. These results suggest that iCDM-34 decreases the phosphorylation of SAMHD1 through CDK1/2, and suppresses HCV replicon RNA, HBV DNA, and pgRNA formation.B型肝炎の完治が見込まれる新たな抗ウイルス薬の候補を発見 --新規の化合物iCDM-34がウイルスゲノムの合成を抑制--. 京都大学プレスリリース. 2023-12-22
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