A high efficiency low noise rf-to-dc converter employing gm-boosting envelope detector and offset canceled latch comparator

This work presents a high efficiency RF-to-DC conversion circuit composed of an LC-CL balun-based Gm-boosting envelope detector, a low noise baseband amplifier, and an offset canceled latch comparator. It was designed to have high sensitivity with low power consumption for wakeup receiver (WuRx) applications. The proposed envelope detector is based on a fully integrated inductively degenerated common-source amplifier with a series gate inductor. The LC-CL balun circuit is merged with the core of the envelope detector by sharing the on-chip gate and source inductors. The proposed technique doubles the transconductance of the input transistor of the envelope detector without any extra power consumption because the gate and source voltage on the input transistor operates in a differential mode. This results in a higher RF-to-DC conversion gain. In order to improve the sensitivity of the wake-up radio, the DC offset of the latch comparator circuit is canceled by controlling the body bias voltage of a pair of differential input transistors through a binary-weighted current source cell. In addition, the hysteresis characteristic is implemented in order to avoid unstable operation by the large noise at the compared signal. The hysteresis window is programmable by changing the channel width of the latch transistor. The low noise baseband amplifier amplifies the output signal of the envelope detector and transfers it into the comparator circuit with low noise. For the 2.4 GHz WuRx, the proposed envelope detector with no external matching components shows the simulated conversion gain of about 16.79 V/V when the input power is around the sensitivity of −60 dBm, and this is 1.7 times higher than that of the conventional envelope detector with the same current and load. The proposed RF-to-DC conversion circuit (WuRx) achieves a sensitivity of about −65.4 dBm based on 45% to 55% duty, dissipating a power of 22 µW from a 1.2 V supply voltage. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.1

Enzymatic production of indigestible maltooligosaccharides using glucansucrases from Leuconostoc mesenteroides B-512FMCM and B-1355CF10

OAIID:RECH_ACHV_DSTSH_NO:A201702459RECH_ACHV_FG:RR00200003ADJUST_YN:EMP_ID:A079459CITE_RATE:FILENAME:동구.pdfDEPT_NM:국제농업기술학과EMAIL:[email protected]_YN:FILEURL:https://srnd.snu.ac.kr/eXrepEIR/fws/file/fe71fb5d-1d6e-4cb2-8b2b-28f93b1bca3c/linkCONFIRM:

Push-Pull Design of Bis(tridentate) Ruthenium(II) Polypyridine Chromophores as Deep Red Light Emitters in Light-Emitting Electrochemical Cells

Breivogel A, Park M, Lee D, et al. Push-Pull Design of Bis(tridentate) Ruthenium(II) Polypyridine Chromophores as Deep Red Light Emitters in Light-Emitting Electrochemical Cells. European Journal of Organic Chemistry. 2014;2014(2):288-295.Light-emitting electrochemical cells (LECs) with a simple device structure were prepared by using heteroleptic bis(tridentate) ruthenium(II) complexes [1](PF6)(2)-[3](PF6)(2) as emitters. The push-pull substitution shifts the emission energy to low energy, into the NIR region. The devices emit deep red light up to a maximum emission wavelength of 755 nm [CIE (International Commission on Illumination) coordinates: x = 0.731, y = 0.269 for [3](PF6)(2)], which, to the best of our knowledge, is the lowest emission energy for LECs containing bis(tridentate) ruthenium(II) complexes. A device structure of ITO/PEDOT:PSS/ruthenium(II) complex/Ag was used, and the thickness of the emitting layer was measured by AFM [ITO: indium tin oxide, PEDOT: poly(3,4-ethylenedioxythiophene), PSS: poly(styrenesulfonate), AFM: atomic force microscopy]. To enhance the external quantum efficiency (EQE), cells were fabricated with and without poly(methyl methacrylate) (PMMA) as additive in the emitting layer

Push-Pull Design of Bis(tridentate) Ruthenium(II) Polypyridine Chromophores as Deep Red Light Emitters in Light-Emitting Electrochemical Cells

Breivogel A, Park M, Lee D, et al. Push-Pull Design of Bis(tridentate) Ruthenium(II) Polypyridine Chromophores as Deep Red Light Emitters in Light-Emitting Electrochemical Cells. European Journal of Organic Chemistry. 2014;2014(2):288-295.Light-emitting electrochemical cells (LECs) with a simple device structure were prepared by using heteroleptic bis(tridentate) ruthenium(II) complexes [1](PF6)(2)-[3](PF6)(2) as emitters. The push-pull substitution shifts the emission energy to low energy, into the NIR region. The devices emit deep red light up to a maximum emission wavelength of 755 nm [CIE (International Commission on Illumination) coordinates: x = 0.731, y = 0.269 for [3](PF6)(2)], which, to the best of our knowledge, is the lowest emission energy for LECs containing bis(tridentate) ruthenium(II) complexes. A device structure of ITO/PEDOT:PSS/ruthenium(II) complex/Ag was used, and the thickness of the emitting layer was measured by AFM [ITO: indium tin oxide, PEDOT: poly(3,4-ethylenedioxythiophene), PSS: poly(styrenesulfonate), AFM: atomic force microscopy]. To enhance the external quantum efficiency (EQE), cells were fabricated with and without poly(methyl methacrylate) (PMMA) as additive in the emitting layer

Precise stacking of decellularized extracellular matrix based 3D cell-laden constructs by a 3D cell printing system equipped with heating modules

Three-dimensional (3D) cell printing systems allow the controlled and precise deposition of multiple cells in 3D constructs. Hydrogel materials have been used extensively as printable bioinks owing to their ability to safely encapsulate living cells. However, hydrogel-based bioinks have drawbacks for cell printing, e.g. inappropriate crosslinking and liquid-like rheological properties, which hinder precise 3D shaping. Therefore, in this study, we investigated the influence of various factors (e.g. bioink concentration, viscosity, and extent of crosslinking) on cell printing and established a new 3D cell printing system equipped with heating modules for the precise stacking of decellularized extracellular matrix (dECM)-based 3D cell-laden constructs. Because the pH-adjusted bioink isolated from native tissue is safely gelled at 37 degrees C, our heating system facilitated the precise stacking of dECM bioinks by enabling simultaneous gelation during printing. We observed greater printability compared with that of a non-heating system. These results were confirmed by mechanical testing and 3D construct stacking analyses. We also confirmed that our heating system did not elicit negative effects, such as cell death, in the printed cells. Conclusively, these results hold promise for the application of 3D bioprinting to tissue engineering and drug development.119Ysciescopu

Mathematical model of STAT signalling pathways in cancer development and optimal control approaches

International audienceIn various diseases, the STAT family display various cellular controls over various challenges faced by the immune system and cell death programs. In this study, we investigate how an intracellular signalling network (STAT1, STAT3, Bcl-2 and BAX) regulates important cellular states, either anti-apoptosis or apoptosis of cancer cells. We adapt a mathematical framework to illustrate how the signalling network can generate a bi-stability condition so that it will induce either apoptosis or anti-apoptosis status of tumour cells. Then, we use this model to develop several anti-tumour strategies including IFN-β infusion. The roles of JAK-STATs signalling in regulation of the cell death program in cancer cells and tumour growth are poorly understood. The mathematical model unveils the structure and functions of the intracellular signalling and cellular outcomes of the anti-tumour drugs in the presence of IFN-β and JAK stimuli. We identify the best injection order of IFN-β and DDP among many possible combinations, which may suggest better infusion strategies of multiple anti-cancer agents at clinics. We finally use an optimal control theory in order to maximize anti-tumour efficacy and minimize administrative costs. In particular, we minimize tumour volume and maximize the apoptotic potential by minimizing the Bcl-2 concentration and maximizing the BAX level while minimizing total injection amount of both IFN-β and JAK2 inhibitors (DDP)

New species of Caromiobenella Jeon, Lee & Soh, 2018 (Crustacea, Copepoda, Monstrilloida) from Chuja Island, Korea

Male monstrilloid copepods belonging to the genus Caromiobenella Jeon, Lee & Soh, 2018 were collected from Chuja Island, Jeju, Korea, using a light trap. This paper describes a new species, Caromiobenella ohtsukai sp. n., based on the display of reduced, knob-like fifth legs on the ventral side of the first urosomal somite. A unique combination of male genitalia features and number of caudal setae further confirms its specificity. Molecular analysis based on two partial gene sequences of mitochondrial cytochrome c oxidase subunit I (mtCOI) and 28S ribosomal RNA (28S rRNA) also supports the designation of this species by showing a relevant divergence from known congeners. Caromiobenella ohtsukai sp. n. is the ninth member of this genus and also the ninth monstrilloid reported from Korea

Role of neutrophil extracellular traps in regulation of lung cancer invasion and metastasis: Structural insights from a computational model.

Lung cancer is one of the leading causes of cancer-related deaths worldwide and is characterized by hijacking immune system for active growth and aggressive metastasis. Neutrophils, which in their original form should establish immune activities to the tumor as a first line of defense, are undermined by tumor cells to promote tumor invasion in several ways. In this study, we investigate the mutual interactions between the tumor cells and the neutrophils that facilitate tumor invasion by developing a mathematical model that involves taxis-reaction-diffusion equations for the critical components in the interaction. These include the densities of tumor and neutrophils, and the concentrations of signaling molecules and structure such as neutrophil extracellular traps (NETs). We apply the mathematical model to a Boyden invasion assay used in the experiments to demonstrate that the tumor-associated neutrophils can enhance tumor cell invasion by secreting the neutrophil elastase. We show that the model can both reproduce the major experimental observation on NET-mediated cancer invasion and make several important predictions to guide future experiments with the goal of the development of new anti-tumor strategies. Moreover, using this model, we investigate the fundamental mechanism of NET-mediated invasion of cancer cells and the impact of internal and external heterogeneity on the migration patterning of tumour cells and their response to different treatment schedules