• Journal of Convergence Korean Medicine
• /
• v.2 no.1
• /
• pp.5-12
• /
• 2021

Objectives: The purpose of this study is to fabricate an ultra-fine ginsenoside particle atomizer that can provide a new treatment method by delivering ginsenoside components that have a therapeutic effect on respiratory diseases directly to the lungs. Methods: We fabricated the AAO vibrating mesh by using the micromachining process. The starting substrate of an AAO wafer has a 350nm pore diameter with 50㎛ thickness. A photomask having several 5㎛ opening holes with a 100㎛ pitch was used to separate each nanopore nozzle. The photoresist structure was optimized to pattern the nozzle area during the lift-off process precisely. The commercial vibrating mesh was removed from OMRON's NE-U100 product, and the fabricated AAO vibrating mesh was installed. A diluted sample of 20mL with 30% red ginseng concentrate was prepared to atomize from the device. Results: As a result of liquid chromatography analysis before spraying the ginsenoside solution, ginsenoside components such as 20S-Rg3, 20R-Rg3, and Rg5 were detected. After spraying through the AAO vibrating mesh, ginsenosides of the same component could be detected. Conclusion: A nutrient solution containing ginsenosides was successfully sprayed through the AAO vibrating mesh with 350 nm selective pores. In particular, during the atomizing experiment of ginsenoside drug solution having excellent efficacy in respiratory diseases, it was confirmed that atomizing through the AAO vibrating mesh while maintaining most of the active ingredients was carried out.

• Nutrition Research and Practice
• /
• v.18 no.4
• /
• pp.464-478
• /
• 2024

BACKGROUND/OBJECTIVES: Chronic alcohol consumption causes oxidative stress in the body, which may accumulate excessively and cause a decline in memory; problem-solving, learning, and exercise abilities; and permanent damage to brain structure and function. Consequently, chronic alcohol consumption can cause alcohol-related diseases. MATERIALS/METHODS: In this study, the protective effects of Phyllostachys edulis (Carrière) J. Houz (PE) against alcohol-induced neuroinflammation and cognitive impairment were evaluated using a mouse model. Alcohol (16%, 5 g/kg/day for 6 weeks) and PE (100, 250, and 500 mg/kg/day for 21 days) were administered intragastrically to mice. RESULTS: PE showed a protective effect against memory deficits and cognitive dysfunction caused by alcohol consumption, confirmed through behavioral tests such as the T-maze, object recognition, and Morris water maze tests. Additionally, PE attenuated oxidative stress by reducing lipid oxidation, nitric oxide, and reactive oxygen species levels in the mice's brains, livers, and kidneys. Improvement of neurotrophic factors and downregulation of apoptosis-related proteins were confirmed in the brains of mice fed low and medium concentrations of PE. Additionally, expression of antioxidant enzyme-related proteins GPx-1 and SOD-1 was enhanced in the liver of PE-treated mice, related to their inhibitory effect on oxidative stress. CONCLUSION: This suggests that PE has both neuroregenerative and antioxidant effects. Collectively, these behavioral and histological results confirmed that PE could improve alcohol-induced cognitive deficits through brain neurotrophic and apoptosis protection and modulation of oxidative stress.

• Journal of Photoscience
• /
• v.9 no.2
• /
• pp.272-274
• /
• 2002

The anterior brain vesicle of ascidian larvae contains two distinct pigment cells. Ultrastructure of these pigment cells has been shown that the anterior pigment cell is an otolith for perception of gravity and the posterior pigment cell is an ocellus for light reception. The larva has remarkably simple central nervous system (CNS) composed of about 330 cells. We focused to study neural networks of visual systems. In the present paper, we report the whole structure of the photoreceptors of the ascidian larva visualized by an antibody against arrestin. Visual arrestin is the key protein for the termination of phototransduction and one of the abundant proteins in photoreceptors. Recently, we cloned an arrestin homologue gene, Ci-arr and the expression of Ci-arr was found to be restricted to the photoreceptors in the ocellus. To study the whole structure of the photoreceptors in the larva, we prepared an antibody against Ci-Arr. It is found that anti Ci-Arr antibody specifically stains the photoreceptors, including the cell bodies, the axons, and the nerve terminals. The photoreceptor cell bodies lies in row outside the pigment cup which penetrate the pigment cell and is continuous with the outer segments of the photoreceptor cell, inside the concavity of the pigments. The axons form bundle into a single tract. The tract extends toward the midline, where the nerve terminals diverge and seem to form synapses

• The Journal of Korean Association of Computer Education
• /
• v.18 no.6
• /
• pp.71-79
• /
• 2015

In a new era of Cloud and Big data, how to search the useful data from dynamic huge data pool in a right time and right way is most important at the stage where the information is getting more important. Above all, in the era of s Big Data it is required to design the advanced efficient intelligent Knowledge system which can process the dynamic variable big data. Accordingly in this paper we propose Dynamic personal Knowledge Network as one of the advanced Intelligent system approach. Adopting the human brain function and its neuro dynamics, an Intelligent system which has a structural flexibility was designed. For Structure-Function association, a personal Knowledge Network is made to be structured and to have reorganizing function as connecting the common nodes. We also design this system to have a reasoning process in the extracted optimal paths from the Knowledge Network.

• Applied Microscopy
• /
• v.48 no.1
• /
• pp.17-26
• /
• 2018

The characteristic features of the arachnid central nervous system (CNS) are related to its body segmentation, and the body in the Opiliones appears to be a single oval structure because of its broad connection between two tagmata (prosoma and opisthosoma). Nevertheless, structural organization of the ganglionic neurons and nerves in the harvestman Leiobunum japonicum is quite similar to the CNS in most other arachnids. This paper describes the fine structural details of the main groups of neuropiles in the CNS ganglia revealed by the transmission electron microscopy. In particular, electron-microscopic features of neural clusters in the main neuroganglia of the CNS (supraesophageal ganglion, protocerebral ganglion, optic lobes, central body, and subesophageal ganglion) could provide indications for the nervous pathways associated with nerve terminations and plexuses. The CNS of this harvestman consists of a supraesophageal ganglion (brain) and a subesophageal mass, and there are no ganglia in the abdomen. Cell bodies of neuroganglia are found in the periphery, but central parts of the ganglia are mostly fibrous in all ganglia. Neuroglial cells occupy the spaces left by nerve cells. Since the nerve cells in the ganglia are typical composed of monopolar neurons, axons and dendrites of neurons are distributed along the same direction.

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 1996.11a
• /
• pp.153-159
• /
• 1996

${\alpha}$-Melanotropin (Ac-Ser-Tyr- Ser-Met-Glu$\^$5/-His-Phe-Arg-Trp-Gly$\^$10/-Lys-Pro-Val-NH$_2$) is one of the first peptide hormones to be isolated and have its structure determined. It was early recognized to have essentially the same N-terminal tridecapeptide sequence as adrenocorticotropic hormone (ACTH) except that the N-terminal was acetylated in the case of ${\alpha}$-MSH but not in the case of ACTH, indicating that their biosyntheses were different (Figure 1). Subsequently it was discovered that ${\alpha}$-MSH and ACTH were derived from the same gene, currently referred to as proopiomelanocortin (POMC). Its original bioactivity was pigmentation, but it also was recognized that it may have activity in the central nervous system, though the precise nature of these central activities have been controversial. The recent cloning and expression of five melanocortin receptors, with the MC3 and MC4 receptors found primarily in the brain and the MC5 receptor (MC5-R) found throughout the body, has provided new impetus to understand the structure-activity relationships of ${\alpha}$-MSH at these receptors. The effects of ${\alpha}$-MSH on pigmentation are mediated by the MC1-R expressed specifically on the surface of melanocytes. Similarly the MC2-R is involved in the regulation of adrenal steroidogenesis by ACTH. However, given the complexity of expression of the MC3, MC4, and MC5 receptors, it has not been possible to identify any simple correlations between these receptors and the reported biological activities of the melanocortin peptides. Consequently, potent and receptor specific agonists and especially antagonists would be extremely valuable tools for the determination of the physiological roles of the MC3, MC4, and MC5 receptors. Though the extensive structure-activity relationships have provided much information on agonist activity related to pigmentary effects, only recently has it been possible to begin to systematically develop potent and selective antagonists.

• Molecules and Cells
• /
• v.37 no.4
• /
• pp.322-329
• /
• 2014

N-acetylglucosamine kinase (GlcNAc kinase or NAGK; EC 2.7.1.59) is highly expressed and plays a critical role in the development of dendrites in brain neurons. In this study, the authors conducted structure-function analysis to verify the previously proposed 3D model structure of GlcNAc/ATP-bound NAGK. Three point NAGK mutants with different substrate binding capacities and reaction velocities were produced. Wild-type (WT) NAGK showed strong substrate preference for GlcNAc. Conversion of Cys143, which does not make direct hydrogen bonds with GlcNAc, to Ser (i.e., C143S) had the least affect on the enzymatic activity of NAGK. Conversion of Asn36, which plays a role in domain closure by making a hydrogen bond with GlcNAc, to Ala (i.e., N36A) mildly reduced NAGK enzyme activity. Conversion of Asp107, which makes hydrogen bonds with GlcNAc and would act as a proton acceptor during nucleophilic attack on the ${\gamma}$-phosphate of ATP, to Ala (i.e., D107A), caused a total loss in enzyme activity. The overexpression of EGFP-tagged WT or any of the mutant NAGKs in rat hippocampal neurons (DIV 5-9) increased dendritic architectural complexity. Finally, the overexpression of the small, but not of the large, domain of NAGK resulted in dendrite degeneration. Our data show the effect of structure on the functional aspects of NAGK, and in particular, that the small domain of NAGK, and not its NAGK kinase activity, plays a critical role in the upregulation of dendritogenesis.

• Proceedings of the Korea Crystallographic Association Conference
• /
• 2003.05a
• /
• pp.18-18
• /
• 2003

Thioredoxin (Trx) is a small redox protein that is ubiquitously distributed from achaes to human. In diverse organisms, the protein is involved in various physiological roles by acting as electron donor and regulators of transcription and apoptosis as well as antioxidants. Sequences of Trx within various species are 27～69% identical to that of E. coli and all Trx proteins have the same overall fold, which consists of central five β strands surrounded by four α helices. The N-terminal cysteine in WCGPC motif of Trx is redox sensitive and the motif is highly conserved. Compared with general cysteine, the N-terminal cysteine has low pKa value. The result leads to increased reduction activity of protein. Recently, novel thio.edoxin-related protein (TRP14) was found from rat brain. TRP14 acts as disulfide reductase like Trx1, and its redox potential and pKa are similar to those of Trx1. However, TRP14 takes up electrons from cytosolic thioredoxin reductase (TrxR1), not from the mitochondrial thioredoxin reductase (TrxR2). Biological roles of TES14 were reported to be involved in regulating TNF-α induced signaling pathways in different manner with Trx1. In depletion experiments, depletion of TRP14 increased TNF-α induced phosphorylation and degradation of IκBα more than the depletion Trx1 did. It also facilitated activation of JNK and p38 MAP kinase induced by TNF-α. Unlike Trx1, TRP14 shows neither interaction nor interference with ASK1. Here, we determined three-dimensional crystal structure of TRP14 by MAD method at 1.8Å. The structure reveals that the conserved cis-Pro (Pro90) and active site-W-C-X-X-C motif, which may be involved in substrate recognition similar to Trx1 , are located at the beginning position of strand β4 and helix α2, respectively. The TRP14 structure also shows that surface of TRP14 in the vicinity of the active site, which is surrounded by an extended flexible loop and an additional short a helix, is different from that of Trx1. In addition, the structure exhibits that TRP14 interact with a distinct target proteins compared with Trx1 and the binding may depend mainly on hydrophobic and charge interactions. Consequently, the structure supports biological data that the TRP14 is involved in regulating TNF-α induced signaling pathways in different manner with Trx1.

• Molecules and Cells
• /
• v.38 no.9
• /
• pp.781-788
• /
• 2015

Mutations of MYO15A are generally known to cause severe to profound hearing loss throughout all frequencies. Here, we found two novel MYO15A mutations, c.3871C>T (p.L1291F) and c.5835T>G (p.Y1945X) in an affected individual carrying congenital profound sensorineural hearing loss (SNHL) through targeted resequencing of 134 known deafness genes. The variant, p.L1291F and p.Y1945X, resided in the myosin motor and IQ2 domains, respectively. The p.L1291F variant was predicted to affect the structure of the actin-binding site from three-dimensional protein modeling, thereby interfering with the correct interaction between actin and myosin. From the literature analysis, mutations in the N-terminal domain were more frequently associated with residual hearing at low frequencies than mutations in the other regions of this gene. Therefore we suggest a hypothetical genotype-phenotype correlation whereby MYO15A mutations that affect domains other than the N-terminal domain, lead to profound SNHL throughout all frequencies and mutations that affect the N-terminal domain, result in residual hearing at low frequencies. This genotype-phenotype correlation suggests that preservation of residual hearing during auditory rehabilitation like cochlear implantation should be intended for those who carry mutations in the N-terminal domain and that individuals with mutations elsewhere in MYO15A require early cochlear implantation to timely initiate speech development.