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This brief presents a high voltage modular supply multiplying pulser in a 0.18- $\mu m$ BCD CMOS process. Two prototypes of the pulser were implemented for target loads of 55pF and 1nF, and generated up to 1MHz and 28.7V pulse from 1.2 and 5V supplies. Proposed modular based stepwise pulse generation achieved a peak power reduction of 75.4% relative to CV 2 f and a peak power efficiency of 82.3%. The proposed pulser was used for driving piezoelectric micromachined ultrasound transducer (pMUT) and achieved a relative efficiency improvement of 113.7% against conventional two-level square wave pulsing.

A multichannel field-programmable gate array (FPGA)-based time-to-digital converter (TDC) and its calibration techniques are presented. Herein, a frequency-tracker-based sliding-scale technique and a moving-average filter to improve the linearity and resolution are proposed. The error calibration technique automatically detects and corrects conversion errors caused by variations and mismatches in the propagation delays. The gain calibration extracts the average bin width of the fine TDC and resolves any linearity degradation in the coarse/fine interpolation architecture. The proposed techniques were applied to a four-channel TDC design implemented on a Xilinx Artix-7 FPGA. The measured differential and integral nonlinearities of all channels were within 0.51 least significant bit of 4.88 ps. The root-mean-squared resolution of the output code was 2.90–8.03 ps across a wide input range of 350 $\mu \text{s}$ .

This paper describes a fully integrated 8-channel front-end module (FEM) single chip IC fabricated with 45-nm RFSOI CMOS process technology for 5G mm-Wave application supporting n257/258/261 triple bands. Its silicon area is 4.29mm × 2.76mm which is comprised of high efficiency Doherty topology power amplifier, low noise amplifier, T/Rx switch, MIPI interface controller and so on. To address module assembly area limitation on the mm-wave antenna PCB, an ultra-thin Embedded Die Substrate (EDS) package is adopted and realizes virtually Zero-space integrate the FEM die in the middle of PCB. The average output power of the Tx is 17dBm with 22% PAE at 5.9% EVM and Rx NF is 3.4dB at the 27GHz.

본 연구는 미등록 이주민의 건강 관리 과정을 살펴보고, 이들의 보건의료서비스 이용에 어떤 장애 요인이 존재하는지 파악한 것이다. 이를 위해 미등록 이주민 14명을 심층 인터뷰하고 근거이론방법으로 분석하였다. 그 결과, 미등록 이주민은 열악한 노동환경에서 일하기 때문에 건강이 나빠지기 쉬운 반면 보건의료서비스를 이용하는데 많은 제약이 존재했다. 사업주가 병원에 가지 못하게 하거나, 의료정보를 얻을 수 있는 곳이 드물었고, 낮은 임금으로 의료비를 지불하기 힘들었다. 더욱이, 비자가 없다는 두려움으로 의료기관에 가는 것을 꺼려 아픈 것을 참는 경향이 컸다. 결국 미등록 이주민들은 건강이 악화한 후에야 보건의료서비스를 이용하는 경우가 많은데, 이 경우에도 의료진과의 언어소통에 어려움을 겪었고, 경우에 따라선 의료진으로부터 불친절하거나 차별적인 대우를 받기까지 했다. 정리하면, 미등록 이주민은 보건의료서비스 이용시, 경제적 요인, 노동환경 요인, 정보 접근성 요인, 무비자(비자 없음), 언어소통의 어려움, 의료진과의 상호작용 문제라는 장벽을 경험했다. 이것을 토대로 4가지 유형을 도출할 수 있었는데, ‘낙관형’, ‘절망형’, ‘체념형’, ‘포기형’이 있었다. 여기에 많은 영향을 준 범주는 ‘경제적 요인’과 ‘언어소통 가능 여부’였다. 그러나 모든 유형에 공통적으로 나타나는 ‘무비자여서 겪는 어려움’과 ‘노동환경 요인’ 역시 고려해야 한다.

A K-band complementary metal-oxide-semiconductor (CMOS) differential cascode power amplifier is designed with the thin-oxide field effect transistor (FET) common source (CS) stage and thick-oxide FET common gate (CG) stage. Use of the thick-oxide CG stage affords the high supply voltage to 3.7 V and enables the high output power. Additionally, simple analysis shows that the gain degradation due to the low cut-off frequency of the thick-oxide CG FET can be compensated by the high output resistance of the thick-oxide FET if the inter-stage node is neutralized. The measured results of the proposed power amplifier demonstrate the saturated output power of the 23.3 dBm with the 31.3% peak power added efficiency (PAE) at 24 GHz frequency. The chip is fabricated in 65-nm low power (LP) CMOS technology and the chip size including all pads is 700 μm × 630 μm.

2-Hydroxy-4-trifluoromethylbenzoic acid (HTB) is a metabolite of triflusal (TF), and has been reported to exert anti-inflammatory effect. In this study, the authors investigated whether HTB has a neuroprotective effect against ischemic brain injuries. We showed that intravenous administration of HTB (5mg/kg) 30min before or 1, 3, or 6h after middle cerebral artery occlusion (MCAO) reduced brain infarct to 10.4±3.3%, 16.9±2.3%, 22.2±1.5% and 40.7±7.5%, respectively, of that of treatment-naive MCAO controls, and the therapeutic time window extended to 9h after MCAO (40.7±7.5%). Furthermore, HTB suppressed infarct formation, protected motor activities, and ameliorated neurological deficits more effectively than by TF or salicylic acid (SA). HTB markedly suppressed microglial activation and proinflammatory cytokines expressions in the postischemic brain and in BV2 cells and suppressed LPS-induced nitrite production by inhibiting IkB degradation. In addition, HTB suppressed NMDA-induced neuronal cell death more effectively than TF or SA in primary cortical neuron cultures. Together, these results indicate that HTB has multi-modal protective effects against ischemic brain damage that encompass anti-inflammatory, anti-excitotoxicity, and anti-Zn2+-toxicity effects.

Fujita Tsuguakira was a man who established Jahyeuiwon, a governmental medical facility, during the Residency-General Period and took over the presidency of a committee in the Japanese Government-General of Chosun after Chosun was annexed to Japanese. In addition, he is a man well qualified to be placed on the top of the list when discussing the Japanese colonial medicine in Chosun, considering his personal history of getting evolved in the colonial rule of Taiwan for seven years as an army surgeon. He led the colonial medicine in Chosun for nine years before and after the Japanese annexation of Korea. He was engaged in almost all the areas related to the colonial medicine such as anti-cholera projects, Hansung Sanitation Union, Deahan Hospital, Chosun Chongdokbu Hospital, Jahyeuiwon, medical schools affiliated to the Japanese Government-General of Chosun. In all respects, his life was in sync with the expansionist strategies of Imperial Japan. Especially, his deeds in Chosun was an "active aid to the instructions" from Army Minister Terauchi Masatake " as Sato Kozo testifies. Fujita was chosen by the military, and so he faithfully served the role given from it. The rewards that he received form the military attest to this fact. He took the position of Surgeon General in Army Medical Service on September, 1912, the top place that an army surgeon could hold. The position was first given to the officer who worked outside Japan proper, and he was the only army surgeon with no doctorial degree to receive such title except for Ishiguro Tadanori who was the first army surgeon in Japan. To sum up, Fujita was not a "doctor" but a "military officer". His walk of life mainly lay in the role of an aider adjusted to the ups and downs and the speeds of the plans of Imperial Japan to invade the continent. Therefore, the Japanese colonial medicine controlled by such man as Fujita in Chosun was inevitably studded with the military things. As a chief in the army medicine, what was important to him was the hospitals for managing the armed troops and projects for preventing infectious disease that could threaten the military sanitation. As a result, the medical service for those under the colonial rule was naturally put on the back burner. This study was conducted mainly based on Fujita's memoirs called Army Surgeon General Fujita Tsuguakira (1943), and accordingly it would be not without limitations. However, as he is a man who cannot be put aside when discussing the Japanese colonial medicine in Chosun, the records by this study of his life and past activities are expected to give no small amount of contribution to these discussions.

// Jong-Ik Heo 1 , Wonwoo Kim 2 , Kyu Jin Choi 1 , Sangwoo Bae 1 , Jae-Hoon Jeong 2 and Kwang Seok Kim 1 1 Divisions of Radiation Effects, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea 2 Research Center for Radiotherapy, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea Correspondence to: Kwang Seok Kim, email: // Keywords : XAF1, p53, ionizing radiation, DNA damage, cellular senescence, BRD7, Gerotarget Received : September 09, 2015 Accepted : January 15, 2016 Published : January 20, 2016 Abstract X-linked inhibitor of apoptosis (XIAP)-associated factor 1 (XAF1) is well known as an antagonist of XIAP-mediated caspase inhibition. Although XAF1 serves as a tumor-suppressor gene, the role of XAF1 in cellular senescence remains unclear. We found that XAF1 expression was increased by genotoxic agents, such as doxorubicin and ionizing radiation in pulmonary microvascular endothelial cells, consequently leading to premature senescence. Conversely, downregulation of XAF1 in premature senescent cells partially overcame endothelial cell senescence. p53 knockdown, but not p16 knockdown, abolished senescence phenotypes caused by XAF1 induction. XAF1 expression was transcriptionally regulated by Bromodomain 7 (BRD7). XAF1 induction with interferon-gamma (IFN-γ) treatment was abrogated by BRD7 knockdown, which resulted in blocking interferon-induced senescence. In lung cancer cells, XAF1 tumor suppressor activity was decreased by BRD7 knockdown, and inhibition of tumor growth by IFN-γ did not appear in BRD7-depleted xenograft tumors. These data suggest that XAF1 is involved in BRD7-associated senescence and plays an important role in the regulation of endothelial senescence through a p53-dependent pathway. Furthermore, regulation of the BRD7/XAF1 system might contribute to tissue or organismal aging and protection against cellular transformation.

Purpose To develop and validate a deep learning system (DLS) for staging liver fibrosis by using CT images in the liver. Materials and Methods DLS for CT-based staging of liver fibrosis was created by using a development data set that included portal venous phase CT images in 7461 patients with pathologically confirmed liver fibrosis. The diagnostic performance of the DLS was evaluated in separate test data sets for 891 patients. The influence of patient characteristics and CT techniques on the staging accuracy of the DLS was evaluated by logistic regression analysis. In a subset of 421 patients, the diagnostic performance of the DLS was compared with that of the radiologist's assessment, aminotransferase-to-platelet ratio index (APRI), and fibrosis-4 index by using the area under the receiver operating characteristic curve (AUROC) and Obuchowski index. Results In the test data sets, the DLS had a staging accuracy of 79.4% (707 of 891) and an AUROC of 0.96, 0.97, and 0.95 for diagnosing significant fibrosis (F2-4), advanced fibrosis (F3-4), and cirrhosis (F4), respectively. At multivariable analysis, only pathologic fibrosis stage significantly affected the staging accuracy of the DLS (P = .016 and .013 for F1 and F2, respectively, compared with F4), whereas etiology of liver disease and CT technique did not. The DLS (Obuchowski index, 0.94) outperformed the radiologist's interpretation, APRI, and fibrosis-4 index (Obuchowski index range, 0.71-0.81; P ˂ .001) for staging liver fibrosis. Conclusion The deep learning system allows for accurate staging of liver fibrosis by using CT images. © RSNA, 2018 Online supplemental material is available for this article.

X-linked inhibitor of apoptosis (XIAP) and Chk1 are potential molecular targets in radiotherapy. However, their molecular association in the regulation of radiation sensitivity has been rarely studied. Here, we show that XIAP modulates radiation sensitivity by regulating stability of Chk1 in lung cancer cells. Both Chk1 and XIAP are highly expressed in various lung cancer cells. Overexpression of XIAP increased cell survival following genotoxic treatments by preventing downregulation of Chk1. However, XIAP reversed Chk1-protective activity in the presence of XIAP-associated factor 1 (XAF1) by degrading Chk1 via ubiquitination-dependent proteasomal proteolysis. The XIAP-XAF1 complex-mediated Chk1 degradation also required CUL4A and DDB1. Chk1 or XIAP was associated with DDB1 and CUL4A. Depletion of CUL4A or DDB1 prevented the XIAP-XAF1-mediated Chk1 degradation suggesting involvement of a CUL4A/DDB1-based E3 ubiquitin ligase in the process or its collaboration with XIAP E3 ligase activity. Taken together, our findings show that XIAP plays a dual role in modulation of Chk1 stability and cell viability following IR. In the absence of XAF1, XIAP stabilizes Chk1 under IR with corresponding increase of cell viability. By contrast, when XAF1 is overexpressed, XIAP facilitates Chk1 degradation, which leads to enhancement of radiation sensitivity. This selective regulation of Chk1 stability by XIAP and XAF1 could be harnessed to devise a strategy to modulate radiation sensitivity in lung cancer cells.

This work presents a 77 GHz radar transmitter for the automotive radar system. An integrated 13 GHz frequency synthesizer fabricated using 130 nm RF CMOS process drives a commercial W-band compound semiconductor monolithic multifunction amplifier(MPA), which includes a frequency multiplier by six to generate 77 GHz transmitting signal. The 13 GHz frequency synthesizer includes a high efficiency injection buffer of 4 dBm output power to drive the MPA. The output power of 77 GHz radar transmitter is higher than 13.99 dBm and the magnitude of the reference spur relative to the carrier is -36.45 dBc. The phase noise is -81 dBc/Hz at 1 MHz offset frequency from the carrier.

Since checkpoint kinase 1 (Chk1) is an essential factor for cell viability following DNA damage, the inhibition of Chk1 has been a major focus of pharmaceutical development to enhance the sensitivity of tumor cells to chemo- and radiotherapy that damage DNA. However, due to the off-target effects of conventional Chk1-targeting strategies and the toxicity of Chk1 inhibitors, alternative strategies are required to target Chk1. To facilitate such efforts, in this study, we identified a specific Chk1-binding 12-mer peptide from the screening of a phage display library and characterized the peptide in terms of cellular cytotoxicity, and in terms of its effect on Chk1 activity and sensitivity to genotoxic agents. This peptide, named N-terminal Chk1-binding peptide (Chk1‑NP), bound the kinase domain of Chk1. Simulation of the binding revealed that the very N-terminus of the Chk1 kinase domain is the potential peptide binding site. Of note, the polyarginine-mediated internalization of Chk1‑NP redistributed nuclear Chk1 with a prominent decrease in the nucleus in the absence of DNA damage. Treatment with Chk1‑NP peptide alone decreased the viability of p53-defective HeLa cells, but not that of p53-functional NCI-H460 cells under normal conditions. The treatment of HeLa or NCI-H460 cells with the peptide significantly enhanced radiation sensitivity following ionizing radiation (IR) with a greater enhancement observed in HeLa cells. Moreover, the IR-induced destabilization of Chk1 was aggravated by treatment with Chk1‑NP. Therefore, the decreased nuclear localization and protein levels of Chk1 seem to be responsible for the enhanced cancer cell killing following combined treatment with IR and Chk1‑NP. The approach using the specific Chk1-binding peptide may facilitate the mechanistic understanding and potential modulation of Chk1 activities and may provide a novel rationale for the development of specific Chk1-targeting agents.

Oncogenic H-Ras G12V and its variants have been shown to inhibit muscle differentiation. However, the role of proto-oncogenic Ras (c-Ras) in muscle differentiation remains unclear. The active GTP-bound form of Ras has been known to associate with diverse effectors including Raf, phosphatidylinositol 3-kinase (PI3K), Ral-GDS, and other molecules to transmit downstream signals. We hypothesize that c-Ras may stimulate muscle differentiation by selectively activating PI3K, an important mediator for muscle differentiation. In our experiments, inhibition of c-Ras by farnesyltransferase inhibitors and a dominant negative form of H-Ras (Ras S17N) suppressed muscle differentiation. Consistently, individual knockdown of H-Ras, K-Ras, and N-Ras by siRNAs all blocked muscle differentiation. Interestingly, we found that c-Ras preferentially interacts with PI3K rather than its major binding partner c-Raf, during myogenic differentiation, with total c-Ras activity remaining unchanged. PI3K and its downstream myogenic pathway, the Nox2/NF-kappaB/inducible nitric oxide synthase (iNOS) pathway, were found to be suppressed by inhibition of c-Ras activity during differentiation. Furthermore, expression of a constitutively active form of PI3K completely rescued the differentiation block and reactivated the Nox2/NF-kappaB/iNOS pathway in c-Ras-inhibited cells. On the basis of our results, we conclude that contrary to oncogenic Ras, proto-oncogenic H-Ras, K-Ras, and N-Ras are directly involved in the promotion of muscle differentiation via PI3K and its downstream signaling pathways. In addition, PI3K pathway activation is associated with a concurrent suppression of the otherwise predominantly activated Raf/Mek/Erk pathway.

The diffusion of I3− in volatile and non-volatile electrolytes is investigated to confirm the effects on the performance of dye-sensitized solar cells (DSSCs). The ionic diffusion is controlled by using electrolyte mediums with diverse viscosities including acetonitrile, 3-methoxy-propionitrile, diethylene glycol dimethyl ether, and poly(ethylene glycol dimethyl ether) with three different molecular weights and varying I3− concentrations. The diffusion flux in each electrolyte is characterized by scanning electrochemical microscopy. By measuring incident photon to current conversion efficiency, electrochemical impedance spectroscopy, and photovoltaic performance, the optimum diffusion flux of I3− is suggested for the best efficiency of DSSCs.

A band-offset-based unified-RAM (URAM) cell fabricated on a Si/Si1-yCy substrate is presented for the fusion of a nonvolatile memory (NVM) and a capacitorless 1T-DRAM. An oxide/nitride/oxide (O/N/O) gate dielectric and a floating-body are combined in a FinFET structure to perform URAM operation in a single transistor. The O/N/O layer is utilized as a charge trap layer for NVM, and the floating-body is used as an excess hole storage node for capacitorless 1T-DRAM. The introduction of a pseudomorphic SiC-based heteroepitaxial layer into the Si substrate provides band offset in a valence band. The FinFET fabricated on the energy-band-engineered Si1-yCy substrate allows hole accumulation in the channel for 1T-DRAM. The band-engineered URAM yields a cost-effective process that is compatible with a conventional body-tied FinFET SONOS. The fabricated URAM shows highly reliable NVM and high-speed 1T-DRAM operations in a single memory cell.

High-performance sub-60 nm Si/SiGe (Ge:~75%)/Si heterostructure quantum well pMOSFETs with a conventional MOSFET process flow, including gate-first high-kappa/metal gate stacks with ~1 nm equivalent oxide thickness, are demonstrated. For the first time, short gate length (L g) devices demonstrate not only controlled short channel effects, but also an excellent on-off current (I on/I off) ratio (~5times104 55-nm L g). The intrinsic gate delay of these heterostructures is ~3 ps at I on/I off~104. OFF-state leakage was minimized by controlling the defects in the epitaxial films. Finally, these short L g devices, when benchmarked against state-of-the-art Si channel pMOSFETs, appear to be very promising in replacing the Si channel in CMOS scaling.

This study measures the diffusion coefficients of I − and I 3 − in oligomer electrolytes as a function of the molecular weight of oligomers and investigates their effect on the performance of dye-sensitized solar cells (DSSCs). The high-diffusion coefficients of ions in an oligomer electrolyte with a lower molecular weight can help to promote the redox mechanism in DSSCs and thereby increase the short-circuit current density. They can also cause a decrease in the open-circuit voltage since a high-diffusion coefficient of I 3 − is capable of reducing the lifetime of electrons in TiO 2 electrodes. To offset these effects, N -methyl-benzimidazole is added to the oligomer electrolytes, thereby improving the open-circuit voltage and fill factor and, consequently, the overall energy-conversion efficiency, which increases to over 5%. A further test involving storage at a high temperature of 75 °C demonstrates that DSSCs employing the oligomer electrolytes show excellent thermal stability over 200 h.

We report a novel Si/Si1-xGex channel with improved current drivability and reliability using a buried Si0.99C0.01. It is also found that the Si/Si1-xGex/Si0.99C0.01 structure is effective in reducing Ge out-diffusion which helps to improve gate dielectric interface quality.

We investigated strain changes in Si1-XGeX layers on silicon substrates upon oxidation. We grew Si1-XGeX layers with different Ge fractions (x=0.15 and 0.3) on chemically cleaned silicon substrates by the UHV CVD process. Oxidation in a vertical furnace at 800C and 900C in an O2 gas ambient produced a silicon oxide layer and a silicon germanium layer that was richer in Ge-content than initial Si1-XGeX films. Initial compressively strained Si1-XGeX films are fully strained in this range of Ge fractions. The strain in the Ge- rich layer increased and then decreased as the oxidation temperature and time increased. In comparison, the strain of the remaining initial Si1-XGeX gradually relaxed with an increase in oxidation time and temperature. The relaxation occurred through the generation of dislocations and defects at the interface of the Si (100) substrate.

Cyclophilin A (CypA) has been reported to be overexpressed in cancer cells, especially in solid tumors. To determine the role of CypA in tumorigenesis, we investigated the induction of CypA as well as the role it plays in cancer cells. Here, we have shown that induction of CypA is associated with hypoxia in a variety of cells, including DU145 human prostate cancer cell line. Our analysis of the CypA promoter clearly showed that CypA up-regulation is mediated by hypoxia-inducible factor-1α transcription factor. Interestingly, overexpression of CypA prevented hypoxia- and cisplatin-induced apoptosis, and this was associated with the suppression of reactive oxygen species generation and depolarization of mitochondrial membrane potential, whereas small interfering RNA–based CypA knockdown aggravated these factors. These results suggest that CypA is important in tumorigenesis, especially in tumor apoptosis. [Cancer Res 2007;67(8):3654–62]