An Examination of the Factors that Influence Drivers’ Willingness to Use the Parking Guidance Information

Yanjie Ji,Pengming Fu,P.T. Blythe,W. Guo,Wei Wang 대한토목학회 2015 KSCE JOURNAL OF CIVIL ENGINEERING Vol.19 No.7

Parking Guidance and Information (PGI) System becomes highly favorable for reducing circulating traffic and making efficient use of existing parking facilities. This paper is to examine the factors influence drivers’ willingness to use PGI. Factor analysis and the Structure Equation Model (SEM) were used to identify the latent attitudinal factors and the sensitivity of the factors was judged by Bayesian network. The heterogeneity of the factors was explored based on driver’s gender, age, driving years, education and travel frequency. The results show that drivers’ willingness to use PGI is significantly correlated to five attitudinal factors: perception of existing PGIs, difficulty in parking, confidence in the accuracy of the information, easy acquisition of information and information attributes. Male drivers, younger drivers, novice drivers and drivers who travel less frequently have lower level of willingness to use PGI.

How Household Roles Influence Individuals’ Travel Mode Choice under Intra-household Interactions?

Yanjie Ji,Yang Liu,Qiyang Liu,Baohong He,Yu Cao 대한토목학회 2018 KSCE JOURNAL OF CIVIL ENGINEERING Vol.22 No.11

The household is usually an essential element for activity-based travel decision-making of individuals. From the perspective of household context, activities are often allocated to individuals based on their household roles, thereby affecting individuals’ travel behavior. By defining the household role using spatial-temporal constraints which are associated with individual activities and household activities, this paper investigates the travel mode choice of individuals considering the effect of different household roles. The descriptive statistics of the household roles and their corresponding travel mode choice are presented using the data from Kunming, China. The statistical results show that the modal splits between females and males perform a significant difference in the same household roles. Furthermore, the travel mode choice of females and males are estimated separately using multinomial logistic regression model. The results show that those who face more space-time constraints associated with household tasks are less willing to travel by car. While with the increase of commuting constraints, household heads, especially female-heads, tend to use car to meet the travel demands of household activity. Besides, individuals’ age, education level, the number of cars and bikes in household also have a significant impact on travel mode choices of individuals.

Nobiletin attenuates neurotoxic mitochondrial calcium overload through K+ influx and ΔΨm across mitochondrial inner membrane

Ji Hyung Lee,Khulan Amarsanaa,Jinji Wu,Sang-Chan Jeon,Yanji Cui,Sung-Cherl Jung,Deok-Bae Park,Se-Jae Kim,Sang-Heon Han,Hyun-Wook Kim,Im Joo Rhyu,Su-Yong Eun 대한생리학회-대한약리학회 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.3

Mitochondrial calcium overload is a crucial event in determining the fate of neuronal cell survival and death, implicated in pathogenesis of neurodegenerative diseases. One of the driving forces of calcium influx into mitochondria is mitochondria membrane potential (ΔΨm). Therefore, pharmacological manipulation of ΔΨm can be a promising strategy to prevent neuronal cell death against brain insults. Based on these issues, we investigated here whether nobiletin, a Citrus polymethoxylated flavone, prevents neurotoxic neuronal calcium overload and cell death via regulating basal ΔΨm against neuronal insult in primary cortical neurons and pure brain mitochondria isolated from rat cortices. Results demonstrated that nobiletin treatment significantly increased cell viability against glutamate toxicity (100 μM,20 min) in primary cortical neurons. Real-time imaging-based fluorometry data reveal that nobiletin evokes partial mitochondrial depolarization in these neurons. Nobiletin markedly attenuated mitochondrial calcium overload and reactive oxygen species (ROS) generation in glutamate (100 μM)-stimulated cortical neurons and isolated pure mitochondria exposed to high concentration of Ca2+ (5 μM). Nobiletininduced partial mitochondrial depolarization in intact neurons was confirmed in isolated brain mitochondria using a fluorescence microplate reader. Nobiletin effects on basal ΔΨm were completely abolished in K+-free medium on pure isolated mitochondria. Taken together, results demonstrate that K+ influx into mitochondria is critically involved in partial mitochondrial depolarization–related neuroprotective effect of nobiletin. Nobiletin-induced mitochondrial K+ influx is probably mediated, at least in part, by activation of mitochondrial K+ channels. However, further detailed studies should be conducted to determine exact molecular targets of nobiletin in mitochondria.

Dieckol Attenuates Microglia-mediated Neuronal Cell Death via ERK, Akt and NADPH Oxidase-mediated Pathways

Yanji Cui,Jee-Yun Park,Jinji Wu,Ji Hyung Lee,Yoon-Sil Yang,Moon-Seok Kang,Sung-Cherl Jung,Joo Min Park,Eun-Sook Yoo,Seong-Ho Kim,Sangmee Ahn Jo,Kyoungho Suk,Su-Yong Eun 대한생리학회-대한약리학회 2015 The Korean Journal of Physiology & Pharmacology Vol.19 No.3

Excessive microglial activation and subsequent neuroinflammation lead to synaptic loss and dysfunction as well as neuronal cell death, which are involved in the pathogenesis and progression of several neurodegenerative diseases. Thus, the regulation of microglial activation has been evaluated as effective therapeutic strategies. Although dieckol (DEK), one of the phlorotannins isolated from marine brown alga <em>Ecklonia cava</em>, has been previously reported to inhibit microglial activation, the molecular mechanism is still unclear. Therefore, we investigated here molecular mechanism of DEK via extracellular signal-regulated kinase (ERK), Akt and nicotinamide adenine dinuclelotide phosphate (NADPH) oxidase-mediated pathways. In addition, the neuroprotective mechanism of DEK was investigated in microglia-mediated neurotoxicity models such as neuron-microglia co-culture and microglial conditioned media system. Our results demonstrated that treatment of anti-oxidant DEK potently suppressed phosphorylation of ERK in lipopolysaccharide (LPS, 1 μg/ml)-stimulated BV-2 microglia. In addition, DEK markedly attenuated Akt phosphorylation and increased expression of gp91^phox, which is the catalytic component of NADPH oxidase complex responsible for microglial reactive oxygen species (ROS) generation. Finally, DEK significantly attenuated neuronal cell death that is induced by treatment of microglial conditioned media containing neurotoxic secretary molecules. These neuroprotective effects of DEK were also confirmed in a neuron-microglia co-culture system using enhanced green fluorescent protein (EGFP)-transfected B35 neuroblastoma cell line. Taken together, these results suggest that DEK suppresses excessive microglial activation and microglia-mediated neuronal cell death via downregulation of ERK, Akt and NADPH oxidase-mediated pathways.

Neuroprotective mechanisms of dieckol against glutamate toxicity through reactive oxygen species scavenging and nuclear factor-like 2/heme oxygenase-1 pathway

Cui, Yanji,Amarsanaa, Khulan,Lee, Ji Hyung,Rhim, Jong-Kook,Kwon, Jung Mi,Kim, Seong-Ho,Park, Joo Min,Jung, Sung-Cherl,Eun, Su-Yong The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.2

Glutamate toxicity-mediated mitochondrial dysfunction and neuronal cell death are involved in the pathogenesis of several neurodegenerative diseases as well as acute brain ischemia/stroke. In this study, we investigated the neuroprotective mechanism of dieckol (DEK), one of the phlorotannins isolated from the marine brown alga Ecklonia cava, against glutamate toxicity. Primary cortical neurons ($100{\mu}M$, 24 h) and HT22 neurons (5 mM, 12 h) were stimulated with glutamate to induce glutamate toxic condition. The results demonstrated that DEK treatment significantly increased cell viability in a dose-dependent manner ($1-50{\mu}M$) and recovered morphological deterioration in glutamate-stimulated neurons. In addition, DEK strongly attenuated intracellular reactive oxygen species (ROS) levels, mitochondrial overload of $Ca^{2+}$ and ROS, mitochondrial membrane potential (${\Delta}{\Psi}_m$) disruption, adenine triphosphate depletion. DEK showed free radical scavenging activity in the cell-free system. Furthermore, DEK enhanced protein expression of heme oxygenase-1 (HO-1), an important anti-oxidant enzyme, via the nuclear translocation of nuclear factor-like 2 (Nrf2). Taken together, we conclude that DEK exerts neuroprotective activities against glutamate toxicity through its direct free radical scavenging property and the Nrf-2/HO-1 pathway activation.

Nobiletin attenuates neurotoxic mitochondrial calcium overload through K⁺ influx and ∆Ψ_m across mitochondrial inner membrane

Lee, Ji Hyung,Amarsanaa, Khulan,Wu, Jinji,Jeon, Sang-Chan,Cui, Yanji,Jung, Sung-Cherl,Park, Deok-Bae,Kim, Se-Jae,Han, Sang-Heon,Kim, Hyun-Wook,Rhyu, Im Joo,Eun, Su-Yong The Korean Society of Pharmacology 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.3

Mitochondrial calcium overload is a crucial event in determining the fate of neuronal cell survival and death, implicated in pathogenesis of neurodegenerative diseases. One of the driving forces of calcium influx into mitochondria is mitochondria membrane potential (${\Delta}{\psi}_m$). Therefore, pharmacological manipulation of ${\Delta}{\psi}_m$ can be a promising strategy to prevent neuronal cell death against brain insults. Based on these issues, we investigated here whether nobiletin, a Citrus polymethoxylated flavone, prevents neurotoxic neuronal calcium overload and cell death via regulating basal ${\Delta}{\psi}_m$ against neuronal insult in primary cortical neurons and pure brain mitochondria isolated from rat cortices. Results demonstrated that nobiletin treatment significantly increased cell viability against glutamate toxicity ($100{\mu}M$, 20 min) in primary cortical neurons. Real-time imaging-based fluorometry data reveal that nobiletin evokes partial mitochondrial depolarization in these neurons. Nobiletin markedly attenuated mitochondrial calcium overload and reactive oxygen species (ROS) generation in glutamate ($100{\mu}M$)-stimulated cortical neurons and isolated pure mitochondria exposed to high concentration of $Ca^{2+}$ ($5{\mu}M$). Nobiletin-induced partial mitochondrial depolarization in intact neurons was confirmed in isolated brain mitochondria using a fluorescence microplate reader. Nobiletin effects on basal ${\Delta}{\psi}_m$ were completely abolished in $K^+-free$ medium on pure isolated mitochondria. Taken together, results demonstrate that $K^+$ influx into mitochondria is critically involved in partial mitochondrial depolarization-related neuroprotective effect of nobiletin. Nobiletin-induced mitochondrial $K^+$ influx is probably mediated, at least in part, by activation of mitochondrial $K^+$ channels. However, further detailed studies should be conducted to determine exact molecular targets of nobiletin in mitochondria.

Dieckol Attenuates Microglia-mediated Neuronal Cell Death via ERK, Akt and NADPH Oxidase-mediated Pathways

Cui, Yanji,Park, Jee-Yun,Wu, Jinji,Lee, Ji Hyung,Yang, Yoon-Sil,Kang, Moon-Seok,Jung, Sung-Cherl,Park, Joo Min,Yoo, Eun-Sook,Kim, Seong-Ho,Ahn Jo, Sangmee,Suk, Kyoungho,Eun, Su-Yong The Korean Society of Pharmacology 2015 The Korean Journal of Physiology & Pharmacology Vol.19 No.3

Excessive microglial activation and subsequent neuroinflammation lead to synaptic loss and dysfunction as well as neuronal cell death, which are involved in the pathogenesis and progression of several neurodegenerative diseases. Thus, the regulation of microglial activation has been evaluated as effective therapeutic strategies. Although dieckol (DEK), one of the phlorotannins isolated from marine brown alga Ecklonia cava, has been previously reported to inhibit microglial activation, the molecular mechanism is still unclear. Therefore, we investigated here molecular mechanism of DEK via extracellular signal-regulated kinase (ERK), Akt and nicotinamide adenine dinuclelotide phosphate (NADPH) oxidase-mediated pathways. In addition, the neuroprotective mechanism of DEK was investigated in microglia-mediated neurotoxicity models such as neuron-microglia co-culture and microglial conditioned media system. Our results demonstrated that treatment of anti-oxidant DEK potently suppressed phosphorylation of ERK in lipopolysaccharide (LPS, $1{\mu}g/ml$)-stimulated BV-2 microglia. In addition, DEK markedly attenuated Akt phosphorylation and increased expression of $gp91^{phox}$, which is the catalytic component of NADPH oxidase complex responsible for microglial reactive oxygen species (ROS) generation. Finally, DEK significantly attenuated neuronal cell death that is induced by treatment of microglial conditioned media containing neurotoxic secretary molecules. These neuroprotective effects of DEK were also confirmed in a neuron-microglia co-culture system using enhanced green fluorescent protein (EGFP)-transfected B35 neuroblastoma cell line. Taken together, these results suggest that DEK suppresses excessive microglial activation and microglia-mediated neuronal cell death via downregulation of ERK, Akt and NADPH oxidase-mediated pathways.

Effects of Nicotine on Aβ or CT_(105)-induced Toxicity

Seo, Ji-Heui,Chang, Keun-A,Kim, Hye-Sun,Park, Cheol Hyoung,Kim, Seong Han,Lee, Me Jeong,Jeong, Sung-Jin,Choi, Se Hoon,Rah, Jong-Cheol,Koo, Jawook,Kim, Eun-Mee,Xu, Yanji,--,Choi, Jun Ho,Shin, Jae Kyung 한국뇌학회 2001 한국뇌학회지 Vol.1 No.1

알츠하이머 치매의 병인기전에서 아밀로이드 베타 펩티드는 중요한 역할을 할 것이라는 연구결과가 많이 보고되어있다. 그러나 알츠하이머 치매의 진행과 아밀로이드 베타 펩티드의 생성에는 여러 가지 모순도 보고되었다. 그러므로 아밀로이드 전구단백질에서 생성된 아밀로이드 베타 펩티드 외에 여러 가지 대사물들이 알츠하이머 치매의 병인기전과 관련이 있으리라 여겨진다. 이미 본 연구팀은 니코틴이 신경보호효과가 있다고 알려진 분비형 아밀로이드 전구단백질의 발현을 시간, 농도 의존적으로 증가시킨다는 연구결과를 보고하였다. 이번 논문에서는 니코틴의 전처리로 아밀로이드 베타 펩티드 및 아밀로이드 C단 단백질에 의한 1차 신경세포에서의 세포독성 효과가 억제되며, 이러한 효과는 니코틴의 길항제인 알파붕가로톡신에 의해 상쇄된다는 연구결과를 얻었다. 뿐만 아니라 C단 단백질을 PC12세포에 유전자를 이입시켰을 때, 니코틴에 의하며 세포 독성이 억제되는 결과를 얻었다. 이러한 연구결과로 볼 때, 니코틴이나 니코틴 수용체는 콜린성 신경전달 물질 보상 뿐만 아니라 아밀로이드 베타 펩티드, 아밀로이드 C단 단백질의 독성을 저해함으로써 인지기능 향상에 영향을 줄 것으로 예상된다. Several lines of evidence indicate that Aβ may play an important role in the pathogenesis of AD. However, there are several discrepancies between the production of Aβ and the development of the disease. Thus, Aβ may not be the sole active fragment of β-amyloid precursor protein (βAPP) in the neurotoxicity associated with AD. Previously, findings from our experiments have shown that nicotine enhances the release of APPs, which has neurotrophic and neuroprotective activities in concentration and time-dependent manners. In this study, our results showed that Pretreatment of nicotine (>10μM, for 24hr) partially prevented Aβ or CT_(105)-induced cytotoxicity in primary cultured neuronal cells, and the effects of nicotine-induced protection was inhibited by the pretreatment with a nicotine receptor antagonist α-bungarotoxin. Nicotine (>10μM, for 24hr) partially inhibited CT_(105)-induced cytotoxicity when PC12 cells was transfected with CT_(105). From these results, we proposed that treatment of nicotine or nicotinic receptor agonist might improve the cognitive functions not only by supplementation of cholinergic neurotransmission but also by protecting Aβ-or CT_(105)-induced neurotoxicity probably through the increased release of APPs and the activation of nicotinic receptor.

What Causes Curbside Illegal Parking Behavior: A Method Based on Structural Equation Model

Jie Yan,Xizhen Zhou,Yanjie Ji 대한토목학회 2023 KSCE Journal of Civil Engineering Vol.27 No.8

Reducing curbside illegal parking is a crucial aspect of urban parking management. However, there is currently a dearth of relevant research. Further analysis is required to determine the factors that influence curbside illegal parking behavior. To this end, a questionnaire survey was conducted in Nanjing, and exploratory factor analysis was used to evaluate the explanatory power of the measurement variables. From this, driver factors, traffic conditions, parking facilities and environment were identified as latent variables. A structural equation model was created to examine the relationship between these variables. The findings indicated that parking facilities and driver factors had a direct and positive correlation with curbside illegal parking behavior, while the environment had a direct and negative correlation with such behavior. Moreover, parking facilities had the greatest impact. The study highlighted the effectiveness of measures such as promoting traffic regulation awareness, optimizing public parking lot charging standards, and strengthening penalties for curbside illegal parking behavior. The results of this research will contribute to a greater comprehension of the phenomenon and provide a theoretical foundation for curbside parking management.

Setosphapyrone C and D accelerate macrophages cholesterol effl ux by promoting LXRa/ABCA1 pathway

Ting Li,Jiayu Yin,Yubin Ji,Ping Lin,Yanjie Li,Zixun Yang,Shumei Hu,Jin Wang,Baihui Zhang,Saloni Koshti,Junfeng Wang,Chenfeng Ji,Shoudong Guo 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.8

LXRα agonists have attracted signifi cant attentiondue to their potential biological activities on promotingcholesterol effl ux. This study was designed to investigatewhether setosphapyrone C and D have potential lipid-loweringcapacity and the underlying mechanisms in vitro. Ourdata showed that setosphapyrone C and D had weak cytotoxicitycompared to the liver X receptor α (LXRα) agonistT0901317. In RAW 264.7 macrophages, setosphapyroneC and D signifi cantly enhanced [ 3 H]-cholesterol effl ux by~ 21.3% and 32.4%, respectively; furthermore, setosphapyroneC and D enhanced the protein levels of ATP-bindingcassette transporter (ABC) A1 and LXRα by 58% and 69%,and 60% and 70% (8 μM), respectively; however, they had noeff ect on the protein levels of ABCG1 and scavenger receptorB type 1; additionally, they had minor eff ect on the mRNAexpression of lipogenic genes. Of note, setosphapyrone C and D signifi cantly enhanced LXRα/ABCA1pathway inmice primary macrophages. In BRL cells, setosphapyroneC and D signifi cantly improved the protein levels of ABCA1and ABCG1; setosphapyrone D signifi cantly enhanced theprotein expression of low-density lipoprotein. Collectively,setosphapyrone C and D with weak cytotoxicity exhibitedeff ective lipid-lowering eff ect via enhancing LXRα/ABCpathways. Setosphapyrones possess potential applicationfor the treatment of hyperlipidemic diseases.