Cold Sputtering Iridium Oxide Films And Their Properties As Impantable Materials For Retinal Electrode

NBS-ERC supported by KOSEF, Kore

Application of the Blister Test to Assess Reliability of Polyimide Based Retinal Electrode

NBS-ERC supported by KOSEF & Korea Health 21 R&D Project(A050251) supported by Ministry of Health & Welfar

Effects of surface ligands on the charge memory characteristics of CdSe/ZnS nanocrystals in TiO2 thin film

harge memory characteristics have been systematically studied based on colloidal CdSe/ZnS nanocrystal quantum dots (QDs) embedded in similar to 50 nm-thick TiO2 film. Ligand-capped QDs showed negligible electron charging effect, implying that the electron affinity of QDs was significantly decreased by surface dipole layer surrounding QDs. In contrast, the hole charging was affected by the carrier injection blocking effect of the surface ligands. Efficient electron and hole charging characteristics were realized by removing the surface ligands via H-2 plasma treatment.open4

Quantum-dot light-emitting diodes utilizing CdSe/ZnS nanocrystals embedded in TiO(2) thin film

Quantum-dot (QD) light-emitting diodes (LEDs) are demonstrated on Si wafers by embedding core-shell CdSe/ZnS nanocrystals in TiO(2) thin films via plasma-enhanced metallorganic chemical vapor deposition. The n-TiO(2)/QDs/p-Si LED devices show typical p-n diode current-voltage and efficient electroluminescence characteristics, which are critically affected by the removal of QD surface ligands. The TiO(2)/QDs/Si system we presented can offer promising Si-based optoelectronic and electronic device applications utilizing numerous nanocrystals synthesized by colloidal solution chemistry.open181

C1-Ten is a PTPase of nephrin, regulating podocyte hypertrophy through mTORC1 activation

Hypertrophy is a prominent feature of damaged podocytes in diabetic kidney disease (DKD). mTORC1 hyperactivation leads to podocyte hypertrophy, but the detailed mechanism of how mTORC1 activation occurs under pathological conditions is not completely known. Moreover, reduced nephrin tyrosine phosphorylation has been observed in podocytes under pathological conditions, but the molecular mechanism linking nephrin phosphorylation and pathology is unclear so far. In this study, we observed a significant increase in C1-Ten level in diabetic kidney and in high glucose-induced damaged podocytes. C1-Ten acts as a protein tyrosine phosphatase (PTPase) at the nephrin-PI3K binding site and renders PI3K for IRS-1, thereby activating mTORC1. Furthermore, C1-Ten causes podocyte hypertrophy and proteinuria by increasing mTORC1 activity in vitro and in vivo. These findings demonstrate the relationship between nephrin dephosphorylation and the mTORC1 pathway, mediated by C1-Ten PTPase activity. We suggest that C1-Ten contributes to the pathogenesis of DKD by inducing podocyte hypertrophy under high glucose conditions.111Ysciescopu

DeepHealthNet: Adolescent Obesity Prediction System Based on a Deep Learning Framework

Childhood and adolescent obesity rates are a global concern because obesity is associated with chronic diseases and long-term health risks. Artificial intelligence technology has emerged as a promising solution to accurately predict obesity rates and provide personalized feedback to adolescents. This study emphasizes the importance of early identification and prevention of obesity-related health issues. Factors such as height, weight, waist circumference, calorie intake, physical activity levels, and other relevant health information need to be considered for developing robust algorithms for obesity rate prediction and delivering personalized feedback. Hence, by collecting health datasets from 321 adolescents, we proposed an adolescent obesity prediction system that provides personalized predictions and assists individuals in making informed health decisions. Our proposed deep learning framework, DeepHealthNet, effectively trains the model using data augmentation techniques, even when daily health data are limited, resulting in improved prediction accuracy (acc: 0.8842). Additionally, the study revealed variations in the prediction of the obesity rate between boys (acc: 0.9320) and girls (acc: 0.9163), allowing the identification of disparities and the determination of the optimal time to provide feedback. The proposed system shows significant potential in effectively addressing childhood and adolescent obesity

Akt regulates the expression of MafK, synaptotagmin I, and syntenin-1, which play roles in neuronal function

<p>Abstract</p> <p>Background</p> <p>Akt regulates various cellular processes, including cell growth, survival, and metabolism. Recently, Akt's role in neurite outgrowth has also emerged. We thus aimed to identify neuronal function-related genes that are regulated by Akt.</p> <p>Methods</p> <p>We performed suppression subtractive hybridization on two previously established PC12 sublines, one of which overexpresses the wild-type (WT) form and the other, the dominant-negative (DN) form of Akt. These sublines respond differently to NGF's neuronal differentiation effect.</p> <p>Results</p> <p>A variety of genes was identified and could be classified into several functional groups, one of which was developmental processes. Two genes involved in neuronal differentiation and function were found in this group. v-Maf musculoaponeurotic fibrosarcoma oncogene homolog K (MafK) induces the neuronal differentiation of PC12 cells and immature telencephalon neurons, and synaptotagmin I (SytI) is essential for neurotransmitter release. Another gene, <it>syntenin-1 </it>(<it>Syn-1</it>) was also recognized in the same functional group into which <it>MafK </it>and <it>SytI </it>were classified. Syn-1 has been reported to promote the formation of membrane varicosities in neurons. Quantitative reverse transcription polymerase chain reaction analyses show that the transcript levels of these three genes were lower in PC12 (WT-Akt) cells than in parental PC12 and PC12 (DN-Akt) cells. Furthermore, treatment of PC12 (WT-Akt) cells with an Akt inhibitor resulted in the increase of the expression of these genes and the improvement of neurite outgrowth. These results indicate that dominant-negative or pharmacological inhibition of Akt increases the expression of <it>MafK</it>, <it>SytI</it>, and <it>Syn-1 </it>genes. Using lentiviral shRNA to knock down endogenous Syn-1 expression, we demonstrated that Syn-1 promotes an increase in the numbers of neurites and branches.</p> <p>Conclusions</p> <p>Taken together, these results indicate that Akt negatively regulates the expression of <it>MafK</it>, <it>SytI</it>, and <it>Syn-1 </it>genes that all participate in regulating neuronal integrity in some way or another.</p

Feasibility of Micro Electrode Array (MEA) Based on Silicone-Polyimide Hybrid for Retina Prosthesis

Purpose: To adopt micropatterning technology in manufacturing silicone elastomer based microelectrode arrays for retinal stimulation, a silicone-polyimide hybrid microelectrode array was proposed and tested in vivo. Methods: Gold microelectrodes were created by semiconductor manufacturing technology based on polyimide, and were hybridized with silicone elastomer by spin coating. The stability of the hybrid between the two materials was flex and blister tested. The feasibility of the hybrid electrode was evaluated in rabbit eye by reviewing optical coherence tomography (OCT) findings after suprachoroidal implantation. Results: The flex test showed no dehiscence between the two materials for 24 h of alternative flexion and extension from -45.0° to +45.0°. During the blister test, delamination was observed at 8.33±1.36 psi of pressure stress; however, this property was improved to 11.50±1.04 psi by oxygen plasma treatment before hybridization. OCT examination revealed that, the implanted electrodes were safely located in the suprachoroidal space during the 4-week follow-up period. Conclusion: The silicone-polyimide hybrid microelectrode array showed moderate physical properties, which are suitable for in vivo application. Appropriate pretreatment before hybridization improved electrode stability. In vivo testing indicated that thiselectrode is suitable as a stimulation electrode in artificial retina.This paper was supported by the Korea Science and Engineering Foundation (KOSEF) through the Nano Bioelectronics and Systems Research Center (NBS-ERC) at Seoul National University, and by a grant from the Korea Health 21 R&D Project(A050251), Ministry of Health & Welfare, Republic of Korea

Syntaphilin controls a mitochondrial rheostat for proliferation-motility decisions in cancer.

Tumors adapt to an unfavorable microenvironment by controlling the balance between cell proliferation and cell motility, but the regulators of this process are largely unknown. Here, we show that an alternatively spliced isoform of syntaphilin (SNPH), a cytoskeletal regulator of mitochondrial movements in neurons, is directed to mitochondria of tumor cells. Mitochondrial SNPH buffers oxidative stress and maintains complex II-dependent bioenergetics, sustaining local tumor growth while restricting mitochondrial redistribution to the cortical cytoskeleton and tumor cell motility. Conversely, introduction of stress stimuli to the microenvironment, including hypoxia, acutely lowered SNPH levels, resulting in bioenergetics defects and increased superoxide production. In turn, this suppressed tumor cell proliferation but increased tumor cell invasion via greater mitochondrial trafficking to the cortical cytoskeleton. Loss of SNPH or expression of an SNPH mutant lacking the mitochondrial localization sequence resulted in increased metastatic dissemination in xenograft or syngeneic tumor models in vivo. Accordingly, tumor cells that acquired the ability to metastasize in vivo constitutively downregulated SNPH and exhibited higher oxidative stress, reduced cell proliferation, and increased cell motility. Therefore, SNPH is a stress-regulated mitochondrial switch of the cell proliferation-motility balance in cancer, and its pathway may represent a therapeutic target