• Journal of Hydrospace Technology
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• v.2 no.1
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• pp.1-9
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• 1996

We consider the following two questions mainly in this study. First one is how the free surface hayes affect the lift of a shallowly submerged moving body. For this matte., we reinterpret the theoretical results of Kochin(1936), and point out that the high Froude number approximation is not always on the safer side. Second one is what sort of dimensionless parameters determine the occurrence of wave breaking behind a moving submerged body. Temporarily before getting a better answer, we propose that the two-parameter-plane, namely, the plane of the Froude number and the square root of the ratio of the submerged depth and the body length, may be used for predicting the possibility of wave breaking behind the submerged body. A region in the parameter plane is put forth as that of wave breaking, and the validity of this proposal is shown by its agreement with the existing experimental data of Parkin et al(1955) and those of Duncan(1983). Finally, linear and nonlinear numerical results are compared with the existing experimental data to see in what range of the parameters the linear and nonlinear theory case predict the wave field and the pressure on the body with reasonable accuracy. However, since the experimental data, which offer both the pressure and wave elevation for a submerged moving body, are very scarce, much cannot be attained through this comparative study. Hence, it is strongly recommended to carry out well planned experiments to get such data.

• BMB Reports
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• v.52 no.4
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• pp.250-258
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• 2019

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by selective and progressive loss of dopaminergic neurons. Genetic and environmental risk factors are associated with this disease. The genetic factors are composed of approximately 20 genes, such as SNCA, parkin, PTEN-induced kinase1 (pink1), leucine-rich repeat kinase 2 (LRRK2), ATP13A2, MAPT, VPS35, and DJ-1, whereas the environmental factors consist of oxidative stress-induced toxins such as 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), rotenone, and paraquat. The analyses of their functions and mechanisms have provided important insights into the disease process, which has demonstrated that these factors cause oxidative damage and mitochondrial dysfunction. The most invaluable studies have been performed using disease model organisms, such as mice, fruit flies, and worms. Among them, Drosophila melanogaster has emerged as an excellent model organism to study both environmental and genetic factors and provide insights to the pathways relevant for PD pathogenesis, facilitating development of therapeutic strategies. In this review, we have focused on the fly model organism to summarize recent progress, including pathogenesis, neuroprotective compounds, and newer approaches.

• BMB Reports
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• v.55 no.10
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• pp.494-499
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• 2022

PTEN-induced putative kinase 1 (PINK1) is a serine/threonine kinase that phosphorylates several substrates and exerts neuroprotective effects against stress-induced apoptotic cell death. Mutations in PINK1 have been linked to autosomal recessive forms of Parkinson's disease (PD). Mitophagy is a type of autophagy that selectively promotes mitochondrial turnover and prevents the accumulation of dysfunctional mitochondria to maintain cellular homeostasis. Toll-interacting protein (Tollip) was initially identified as a negative regulator of IL-1β receptor signaling, suppressing inflammatory TLR signaling cascades. Recently, Tollip has been reported to play a role in autophagy and is implicated in neurodegeneration. In this study, we determined whether Tollip was functionally linked to PINK1-mediated mitophagy. Our results demonstrated that Tollip promoted the mitochondrial processing of PINK1 and altered the localization of PINK1, predominantly to the cytosol. This action was attributed to increased binding of PINK1 to mitochondrial processing peptidase β (MPPβ) and the subsequent increase in MPPβ-mediated mitochondrial PINK1 cleavage. Furthermore, Tollip suppressed mitophagy following carbonyl cyanide m-chlorophenylhydrazone-induced mitochondrial dysfunction. These findings suggest that Tollip inhibits mitophagy via the PINK1/parkin pathway upon mitochondrial damage, leading to the blockade of PINK1-mediated neuroprotection.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.4
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• pp.2643-2647
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• 2013

Background: Despite anti-smoking campaigns, smoking prevalence among Thai males aged 30 or older is high, at around 50%. The purpose of this study was to determine the relationship between smoking and mortality in a rural Thai community. Materials and Methods: Subjects enrolled into the Khon Kaen cohort study between 1990 and 2001 were followed up for their vital status until $16^{th}$ March 2012. The death resource was from the Bureau of Policy and Strategy, Ministry of Interior, Thailand. A Cox proportional hazards model was used to analyse the association between smoking and death, controlling for age, education level and alcohol drinking, and confidence intervals were calculated using the floating risk method. Results: The study recruited 5,962 male subjects, of whom 1,396 died during a median 13.5 years of follow-up. Current smokers were more likely to die than never smokers after controlling for age, education level and alcohol drinking (HR, 95%CI: 1.41, 1.32-1.51), and the excess mortality was greatest for lung cancer (HR, 95%CI: 3.51, 2.65-4.66). However, there was no increased risk with increasing dose of tobacco, and no difference in risk between smokers of yamuan (hand-rolled cigarettes) and manufactured tobacco. Conclusion: Mortality from cancer, particularly lung cancer, and from all causes combined is dependent on smoking status among men in rural Thailand, but the relative risks are lower than have been reported from studies in high income countries, where the tobacco epidemic is more established.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.3
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• pp.223-232
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• 2020

Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G₀/G₁ phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.8
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• pp.3413-3418
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• 2015

Background: Liver fluke infection caused by the parasite Opisthorchis viverrini (O. viverrini), a human carcinogen, is endemic in north-eastern Thailand and remains a major health problem. Objectives: The objectives of the study were to (1) resurvey the prevalence of O. viverrini infection in a field site from the Khon Kaen Cohort Study (in newly recruited subjects as well as previous cohort subjects surveyed in 1992); (2) investigate how subjects' lifestyle habits and their exposure to health promotion initiatives influence changes in prevalence of O. viverrini infection. Materials and Methods: The prevalence of O. viverrini infection in the cohort subjects (as well as new subjects) was investigated using faecal egg counts. Information on demographic factors, lifestyle and awareness of health promotion initiatives were obtained through questionnaires. Results: O. viverrini infection rates in the same individuals of the cohort were lower in 2006 than in 1992. Also, by studying the period effect, the current 35-44 year olds had a 12.4% (95% CI 3.9% to 20.9%) lower prevalence of O. viverrini infection than the 35-44 year olds in 1992 (24.2% versus 11.8%). Lifestyle choices showed that smoking and alcohol consumption were associated with an increased chance of acquiring O. viverrini infection with adjusted odds ratios of 10.1 (95%CI 2.4-41.6) and 5.3 (95%CI 1.2-23.0), respectively. Conclusions: Our study has demonstrated that although the prevalence of O. viverrini infection over a 14-year period has decreased, unhealthy lifestyle was common with smoking and alcohol consumption being associated with increased chances of infection, emphasising the double burden of disease which developing countries are facing.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2007.04a
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• pp.147-153
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• 2007

Central to developing new treatment strategies for late onset sporadic Parkinson's disease (PD) and early onset familial PD is resolving the enigma of the specific vulnerability exhibited by substantia nigra dopamine (DA) neurons despite multiple risk factors. Neuropathological evidence from both human and experimental models of PD firmly supports a significant role for oxidative stress (OS) and mitochondrial dysfunction in the death of nigral DA neurons. Largely unknown are the genes underlying selective susceptibility of nigral DA neuron to OS and mitochondrial dysfunction and how they effect nigral DA cell death. To overcome the paucity of nigral DA neurons as well as the dilution effect of non-DA cells in brain tissues, we have developed wild type DA cell line model, SN4741 and mutant DJ-1 (-/-) DA cells, appropriate for microarray analysis and differential mitochondrial proteomics. Mutations in the DJ-1 gene (PARK7), localized in cytoplasm and mitochondria, cause autosomal recessive early onset PD. Through microarray analysis using SN4741 cells followed by validation tests, we have identified a novel phylogenically conserved neuroprotective gene, Oxi-a, which is specifically expressed in DA neurons. The knockdown of the gene dramatically increased vulnerability to as. Importantly as down-regulated the expression level of the gene and recovery of its expression via transient transfection exerted significant neuroprotection against as insult. We also have identified altered expression of mitochondrial proteins and other familial PD genes in DJ-1 (-/-) mutant cells by differential mitochondrial proteomics. In DJ-1 (-/-) cells the knockdown of the other familial PD genes (Parkin and PINK1) dramatically increased susceptibility to as. Thus, further functional characterization of the Oxi-$\alpha$ gene family and the mitochondrial alteration in the DJ-1 (-/-) cell model will provide the rationale for the neuroprotective therapy against both sporadic and familial PD.

• The Korean Journal of Nuclear Medicine Technology
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• v.19 no.1
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• pp.67-71
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• 2015

Purpose At recently, we enter into the aging society and a age-related disease is increasing. Among that, prevalence of degenerative brain disease like Parkin's disease will be increased. So, many radiopharmaceuticals is developed to diagnosis early and to evaluate the performance of therapeutic drugs. Especially $^{18}F-DOPA$ which involved at dopamine synthesis and function of storage is widely used to the diagnosis of Parkinson's disease as well as brain tumors. in the study, we will evaluate the distribution pattern of $^{18}F-DOPA$ at the striatum by using dynamic study. Materials and Methods We used Biograph Truepoint(Siemens, Germany) as PET/CT scanner, injected a $^{18}F-DOPA$ ($600{\pm}30MBq$) to patient (4men, 6women. $67{\pm}11age$) who visited our hospital from June to September, started 95min dynamic study at same time. after finishing acquisition, we reconstructed PET data with 19 frame every 5 minutes, analysed a average counts at ROI's where set at both striatums, anterior putamen, posterior putamen Results Counts in the cerebellum as the background formed a plateau after 90 minutes from the highest out rapidly reduced to 15 minutes. Counts of anterior putamen and posterior gradually increased but formed a plateau after 60min. A count ratio of Striatum to cerebellum was continuously increased up to more than 95 minutes, A count ratios of an anterior putamen to posterior one formed a plateau after 85 minutes. Conclusion The dynamic acquisition can be possible to evaluate a distribution of the $^{18}F-DOPA$ in the striatum and the VOI analysis through a dynamic acquisition and a variety of patterns. Futhermore, to make a uniformed distribution and count ratio of striatum to cerebellum, a static acquisition will have to start 90minutes later after injection.

• Journal of Animal Science and Technology
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• v.63 no.4
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• pp.766-777
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• 2021

Bezafibrate, a fibrate drug used as a lipid-lowering agent to treat hyperlipidemia, is a pan-agonist of peroxisome proliferator-activated receptor alpha. It can enhance mitochondrial fatty acid oxidation, oxidative phosphorylation, and mitochondrial biogenesis. After ovulation, oocytes may get arrested at the metaphase II (MII) stage until fertilization beyond optimal timing, which is termed as post-ovulatory aging. Post-ovulatory aging is a disease that degrades DNA, mitochondria, and oxidative system, and has a negative impact on embryo development and quality; however, the impact of bezafibrate during post-ovulatory aging has not been fully defined. In the present study, we assessed the ability of bezafibrate to prevent the progression of aging in in vitro conditions as well as the underlying mechanisms in pigs. An appropriate concentration of this drug (50 µM) was added, and then oxidative stress, reactive oxygen species downstream, mitochondrial biogenesis, and mitochondrial function were analyzed via immunofluorescence staining and real-time polymerase chain reaction. Bezafibrate significantly alleviated reactive oxygen species and ameliorated glutathione production simultaneously in oocytes and embryos. Moreover, it diminished H2A.X and attenuated CASPASE 3 expression produced by oxidative stress in oocytes and embryos. Furthermore, bezafibrate remarkably improved the mitochondrial function and blastocyst quality as well as markedly reduced the mitochondria/TOM20 ratio and mtDNA copy number. The elevated PARKIN level indicated that mitophagy was induced by bezafibrate treatment after post-ovulatory aging. Collectively, these results suggest that bezafibrate beneficially affects against porcine post-ovulatory oocyte aging in porcine by its antioxidant property and mitochondrial protection.

• The Journal of Internal Korean Medicine
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• v.41 no.6
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• pp.1089-1099
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• 2020

Objective: The purpose of this study was to investigate the effect of cinnamon on the treatment of Parkinson's disease (PD) and to introduce its use in Korea. Method: We searched the experimental studies in electronic databases (PubMed, CNKI, Wanfang, CiNii, J-STAGE, Science ON, and OASIS) using the key search terms "cinnamic acid", "cinnamon", "cinnamomum", "Parkinson's disease", "Parkinson disease", "Parkinsonism", and "dopamine". This study only involved experimental studies (in vivo and in vitro) that adopted cinnamon as a single administration and measured indicators relating to Parkinson's disease, including parkin, tyrosine hydroxylase (TH), and dopamine. Results: A Total of 11 literature studies were selected, and they all showed that treatment with cinnamon has a neuroprotective effect. Cinnamon activated neuroprotective factors and restored neurotransmitters and it reduced the rate of oxidative stress and inflammation in neurons. As a result, cell viability was upregulated, while cell apoptosis and neurodegeneration were downregulated. Five in vivo studies, through behavioral tests, also confirmed that cinnamon recovers locomotor function in PD models. Conclusion: We identified that cinnamon is an effective neural protector and improves motor performance in behavioral testing in the experimental PD studies.