Delving into the Latest Updates on Dong-A University with Synapse

Effects of virtual reality-based breathing training on recovering pulmonary function and preventing postoperative pulmonary complications in post-laparotomy patients

开始日期2024-06-07

申办/合作机构

Dong-A University

KCT0009099

/ Recruiting临床3期IIT

Comparison of postoperative pain control in patients undergoing laparoscopic cholecystectomy after performing right subcostal TAP block, bilateral subcostal TAP block, and 4-point TAP block

开始日期2023-01-03

申办/合作机构

Dong-A University

KCT0008053

/ Recruiting临床3期IIT

A Comparison of effect of preemptive versus post-operative rectus sheath block (RSB) on robotic cholecystectomy

开始日期2023-01-03

申办/合作机构

Dong-A University

100 项与 Dong-A University 相关的临床结果

登录后查看更多信息

0 项与 Dong-A University 相关的专利（医药）

登录后查看更多信息

10,742

项与 Dong-A University 相关的文献（医药）

2025-12-31·Animal Cells and Systems

Loss of neuronal βPix isoforms impairs neuronal morphology in the hippocampus and causes behavioral defects

Article

作者: Park, Dongeun ; Choi, June-Seek ; Lee, Seung Joon ; Shin, Yoon Kyung ; Kwon, Younghee ; Shin, Jung Eun

βPix is a guanine nucleotide exchange factor for the Rac1 and Cdc42 small GTPases, which play important roles in dendritic spine morphogenesis by modulating actin cytoskeleton organization. The formation and plasticity of the dendritic spines are essential for normal brain function. Among the alternatively spliced βPix isoforms, βPix-b and βPix-d are expressed specifically in neurons. Our previous studies using cultured hippocampal neurons identified the roles of βPix-b and βPix-d in spine formation and neurite development, respectively. Here, we analyzed the in vivo role of the neuronal βPix isoforms in brain development and function by using βPix neuronal isoform knockout (βPix-NIKO) mice, in which the expression of the βPix-b and βPix-d isoforms is blocked, while the expression of the ubiquitous βPix-a isoform is maintained. Loss of the neuronal βPix isoforms leads to reduced activity of Rac1 and Cdc42, decreased dendritic complexity and spine density, and increased GluN2B and Ca²⁺/calmodulin-dependent protein kinase IIα expression in the hippocampus. The defects in neurite development, dendritic spine maturation, and synaptic density in cultured βPix-NIKO hippocampal neurons were rescued by the expression of βPix-b or βPix-d. In behavioral studies, βPix-NIKO mice exhibited robust deficits in novel object recognition and decreased anxiety levels. Our findings suggest that neuronal morphogenetic signaling by the neuronal βPix isoforms contributes to normal behaviors.

2025-08-01·Toxicology

Particulate matter 2.5 stimulates pyroptosis and necroptosis via the p38 MAPK/Akt/NF-κB signaling pathway in human corneal epithelial cells

Article

作者: Kim, Gi Young ; Kim, Da Hye ; Kim, Min Yeong ; Choi, Yung Hyun ; Leem, Sun-Hee ; Ryu, Dongryeol ; Hwangbo, Hyun ; Cheong, JaeHun ; Lee, Hyesook ; Bang, EunJin ; Ji, Seon Yeong ; Hong, Su Hyun

Particulate matter 2.5 (PM_2.5) exposure poses significant health risks, particularly to the eyes. This study aimed to investigate the cytotoxic effects of PM_2.5 on human corneal epithelial cells (HCECs) and to elucidate the mechanisms involved in pyroptosis and necroptosis. HCECs were exposed to PM_2.5, and cytotoxicity, reactive oxygen species (ROS) levels, and the expression of pyroptosis- and necroptosis-related proteins were assessed. The roles of nuclear factor-kappa B (NF-κB) and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome signaling pathways were also investigated. Exposure to PM_2.5 caused a dose-dependent decrease in cell viability, accompanied by significant NLRP3 inflammasome activation, leading to pyroptosis and the release of pro-inflammatory cytokines. Enhanced ROS generation and mitochondrial dysfunction have also been observed, along with indicators of necroptosis, such as increased levels of mixed-lineage kinase domain-like proteins. Importantly, activation of the NF-κB signaling pathway was crucial for these responses. The suppression of p38 mitogen-activated protein kinase (MAPK) and activation of protein kinase B (Akt) using pharmacological modulators SB203580 and SC79, respectively, significantly reduced PM_2.5-mediated cellular damage. These findings indicate that p38 MAPK inhibition and Akt activation are key regulatory mechanisms that help attenuate the deleterious effects of PM_2.5 on HCECs. In conclusion, our findings offer new insights into the mechanisms by which PM_2.5 induces pyroptosis and necroptosis in HCECs, especially by activating the NLRP3 inflammasome and NF-κB signaling pathways. The critical regulatory roles of p38 MAPK and Akt underscore their potential as therapeutic targets to alleviate PM-induced ocular damage.

2025-07-01·Neuropharmacology

Chronic stress-related behavioral and synaptic changes require caspase-3 activation in the ventral hippocampus of male mice

Article

作者: Shin, Chan Young ; Moon, Somin ; Kim, Dong Hyun ; Kwon, Kyoung Ja ; Yi, Jee Hyun ; Kwon, Hyun Ji ; Jeon, Jieun ; Kwon, Huiyoung ; Cho, Eunbi ; Park, A Young ; Ryu, Jong Hoon

Although numerous studies have suggested that chronic stress is a major risk factor for major depressive disorder, the process by which stress causes depression is still not fully understood. Previously, we investigated glucocorticoids, which are stress response hormones that activate a synapse-weakening pathway. Therefore, we hypothesized that chronic stress may cause synaptic depression, which could reduce excitability related to emotions. Animals underwent chronic restraint stress (CRS), followed by basal synaptic transmission measurement in hippocampal slices to assess synaptic function. Drugs were infused into the ventral hippocampus via cannulation before behavioral tests, including forced swimming, tail suspension, and sucrose intake tests, which evaluated depressive-like behaviors and anhedonia. The field excitatory postsynaptic potentials (fEPSPs) are reduced by chronic restraint stress (CRS) in the ventral hippocampus. The ventral hippocampi of mice treated with CRS showed low levels of fEPSP after the forced swim test (FST). In the FST and tail suspension test, CRS-induced increases in immobility time were prevented by the acute inhibition of AMPAR internalization by Tat-GluA2_3y, which also prevented fEPSP reduction. Mice lacking caspase-3 exhibited resilience to CRS-induced increases in immobility time in the FST, as well as changes in the functionality of synaptic AMPAR. Finally, the caspase-3 inhibitor Z-DEVD-FMK rapidly blocked the CRS-induced increase in immobility time in the FST and the CRS-induced decrease in sucrose preference. These findings suggest that chronic stress-related behavioral changes may require caspase-3-dependent alterations in ventral hippocampal synapses.

100 项与 Dong-A University 相关的药物交易

登录后查看更多信息

100 项与 Dong-A University 相关的转化医学

登录后查看更多信息

组织架构

使用我们的机构树数据加速您的研究。

登录

或

查看完整样例数据

管线布局

2025年05月15日管线快照

管线布局中药物为当前组织机构及其子机构作为药物机构进行统计，早期临床1期并入临床1期，临床1/2期并入临床2期，临床2/3期并入临床3期

临床前

3

登录后查看更多信息

当前项目

药物(靶点)	适应症	全球最高研发状态

15d-PGJ2 ( Akt x PPARγ )	白血病更多	临床前
Derivative 10b(Palacký University) ( FLT3 )	创伤和损伤更多	临床前
Compound 8a(Dong-A University) ( RdRp )	SARS-CoV-2 急性呼吸道疾病更多	临床前