Jin-Hyeok Choi

Electron mobility behavior in extremely thin SOI MOSFET's

Extremely thin-film SOI MOSFETs with silicon film thickness down to 8 nm have been fabricated without inducing serious source/drain series resistance by employing a gate recessed structure. The influence of extremely thin silicon film on the electron mobility has been experimentally studied. The results show an abrupt mobility decrease in the device with less than 10 nm silicon film thickness. The measured mobility versus effective field below 10 nm silicon film thickness shows that a different scattering mechanism is involved in carrier conduction in 10 nm t/sub si/ region. The reasons for the mobility decrease have been examined from a device simulation and measurements. >

Body-contacted SOI MOSFET structure with fully bulk CMOS compatible layout and process

A new SOI MOSFET structure to reduce the floating body effect is proposed and successfully demonstrated. The key idea of the proposed structure is that the field oxide does not consume the silicon film completely, so that the well contact can suppress the body potential increase in SOI MOSFET through the remaining silicon film between the field oxide and buried oxide. The measured results show the suppressed floating body effect as expected. This new structure retains most of the advantages in the propagation delay of the conventional SOI MOSFET without body potential instability. An additional advantage of the proposed structure is that the layout and process are the same as those of bulk CMOS.

Improvement of breakdown voltage in SOI n-MOSFETs using the gate-recessed (GR) structure

A gate-recessed structure is introduced to SOI MOSFETs in order to increase the source-to-drain breakdown voltage. A significant increase in the breakdown voltage can be seen compared with that of a planar single source/drain SOI MOSFET without inducing the appreciable reduction of the current drivability. We have analyzed the origin of the breakdown voltage improvement by the substrate current measurements and 2-D device simulations, and shown that the breakdown voltage improvement is caused by the reductions in the impact ionization rate and the parasitic bipolar current gain.

A‑kinase anchoring protein 12 is downregulated in human hepatocellular carcinoma and its deficiency in mice aggravates thioacetamide‑induced liver injury

AKAP12 belongs to A-kinase anchoring protein (AKAP) family of scaffold proteins and is known as a tumor suppressor in several human cancer types. Its role as a tumor suppressor in hepatocellular carcinoma (HCC) was proposed due to its downregulation and epigenetic modification in human HCC; however, the effect of its deficiency on liver injuries, such as liver fibrosis and cancer has been poorly studied. By analyzing tumor and non-tumor tissues of 15 patients with HCC, it was confirmed that AKAP12 expression was downregulated in human HCC as compared with adjacent non-tumor tissues. Immunohistochemical staining of mouse liver tissue for AKAP12 revealed that its sinusoidal expression was diminished in capillarized endothelium after 8 weeks of thioacetamide (TAA) administration. AKAP12 deficiency resulted in the promotion of ductular response of biliary epithelial cells, whereas overall fibrosis and myofibroblast activation were comparable between genotypes after short-term TAA treatment. The mRNA expressions of some fibrosis-related genes such as those encoding epithelial cell adhesion molecule, collagen type 1 α1 and elastin were upregulated in liver tissues of AKAP12-knockout mice. Long-term administration of TAA for 26 weeks led to the development of liver tumors; the incidence of tumor development was higher in AKAP12-deficient mice than in wild-type littermates. Together, these results suggest that AKAP12 functions as a tumor suppressor in liver cancer and is associated with the regulation of hepatic non-parenchymal cells.

Altered AKAP12 expression in portal fibroblasts and liver sinusoids mediates transition from hepatic fibrogenesis to fibrosis resolution

Liver fibrosis can be reversed by removing its causative injuries; however, the molecular mechanisms mediating the resolution of liver fibrogenesis are poorly understood. We investigate the role of a scaffold protein, A-Kinase Anchoring Protein 12 (AKAP12), during liver fibrosis onset, and resolution. Biliary fibrogenesis and fibrosis resolution was induced in wild-type (WT) or AKAP12-deficient C57BL/6 mice through different feeding regimens with 0.1% 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-containing chow. AKAP12 expression in portal fibroblasts (PFs) and liver sinusoidal endothelial cells (LSECs) gradually decreased as fibrosis progressed but was restored after cessation of the fibrotic challenge. Histological analysis of human liver specimens with varying degrees of fibrosis of different etiologies revealed that AKAP12 expression diminishes in hepatic fibrosis from its early stages onward. AKAP12 KO mice displayed reduced fibrosis resolution in a DDC-induced biliary fibrosis model, which was accompanied by impaired normalization of myofibroblasts and capillarized sinusoids. RNA sequencing of the liver transcriptome revealed that genes related to ECM accumulation and vascular remodeling were mostly elevated in AKAP12 KO samples. Gene ontology (GO) and bioinformatic pathway analyses identified that the differentially expressed genes were significantly enriched in GO categories and pathways, such as the adenosine 3′,5′-cyclic monophosphate (cAMP) pathway. Knockdown of the AKAP12 gene in cultured primary PFs revealed that AKAP12 inhibited PF activation in association with the adenosine 3′,5′-cyclic monophosphate (cAMP) pathway. Moreover, AKAP12 knockdown in LSECs led to enhanced angiogenesis, endothelin-1 expression and alterations in laminin composition. Collectively, this study demonstrates that AKAP12-mediated regulation of PFs and LSECs has a central role in resolving hepatic fibrosis.Liver fibrosis: Reversing the damageA scaffolding protein that modulates cell signaling pathways contributes to reverse liver scarring. Liver fibrosis is caused by a build-up of scar tissue that interferes with liver function. However, the damage is reversed when the cause of injury is removed. Kyu-Won Kim at Seoul National University, South Korea, and colleagues examined the levels of A-Kinase Anchoring Protein 12 (AKAP12), a scaffolding protein that regulates the subcellular location of signaling proteins, in mouse and human livers. Levels of AKAP12 were reduced in fibrotic livers but restored when fibrosis was reversed. Mice lacking AKAP12 were unable to effectively repair the damage caused by fibrosis. Genetic analyses suggest that AKAP12 stimulates signaling through the adenosine 3′,5′-cyclic monophosphate (cAMP) pathway, which can inhibit fibrosis. These findings highlight a key role for AKAP12 in accelerating liver recovery.

Implementation of time-efficient adaptive sampling function design for improved undersampled MRI reconstruction.

To improve the efficacy of undersampled MRI, a method of designing adaptive sampling functions is proposed that is simple to implement on an MR scanner and yet effectively improves the performance of the sampling functions. An approximation of the energy distribution of an image (E-map) is estimated from highly undersampled k-space data acquired in a prescan and efficiently recycled in the main scan. An adaptive probability density function (PDF) is generated by combining the E-map with a modeled PDF. A set of candidate sampling functions are then prepared from the adaptive PDF, among which the one with maximum energy is selected as the final sampling function. To validate its computational efficiency, the proposed method was implemented on an MR scanner, and its robust performance in Fourier-transform (FT) MRI and compressed sensing (CS) MRI was tested by simulations and in a cherry tomato. The proposed method consistently outperforms the conventional modeled PDF approach for undersampling ratios of 0.2 or higher in both FT-MRI and CS-MRI. To fully benefit from undersampled MRI, it is preferable that the design of adaptive sampling functions be performed online immediately before the main scan. In this way, the proposed method may further improve the efficacy of the undersampled MRI.

Real-time generation of fast, torque-efficient motions

We present a method for generating fast, torque-efficient motions in real-time. Given a dynamic model of a robot, we first obtain a reasonably large set of minimum torque motions for arbitrary starting and ending configurations, that also achieve minimum time without actuator saturation; these motions are obtained through a Lie group dynamics-based optimization procedure previously developed by the authors. After classifying the minimum torque motions according to the region of the workspace traversed, a principal component analysis is performed for each class of motions. The dominant principal components are then used as basis functions in a simple interpolating scheme for generating torque-efficient motions between arbitrary starting and ending configurations. Results obtained for a typical industrial manipulator clearly demonstrate the performance advantages over traditional spline interpolation methods