• Asian-Australasian Journal of Animal Sciences
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• v.21 no.7
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• pp.988-994
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• 2008

The purpose of the investigation was to establish how the pineal-adrenal axis plays an important role in thermoregulation in female goats under short-term heat stress. The study was conducted to observe the influence of glucocorticoids on pineal function in goats and its influence on stress alleviation capability. Melatonin and glucocorticoid secretions and several other endocrine and biochemical blood parameters reflecting the animals well being were determined over a one week period after goats had been exposed to $40^{\circ}C$ and 60% relative humidity for 10 days. Six female goats were used in the study. These animals served as self controls prior to the start of the experiment. The study was conducted for a period of seventeen days in a psychrometric chamber at $40^{\circ}C$ and 60% relative humidity. Chemical pinealectomy was achieved using propranolol followed by exogenous hydrocortisone treatment. Blood samples were drawn twice daily after each treatment to find the effect of hydrocortisone on plasma glucose, total protein, total cholesterol, cortisol, insulin, aldosterone, melatonin and corticosterone. Chemical pinealectomy significantly ($p{\leq}0.05$) affected plasma levels of the parameters studied and these could be significantly ($p{\leq}0.05$) counteracted by administration of hydrocortisone. Chemical pinealectomy aggravated thermal stress, although administration of hydrocortisone could ameliorate the condition. This indicated a role of the pineal in support of thermoregulation. The study establishes the modulating effect of glucocorticoids on pineal activity to relieve thermal stress in goats.

• Korean Journal of Veterinary Research
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• v.44 no.4
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• pp.497-505
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• 2004

The proliferation of mesangial cells has been associated with the development of diabetic nephropathy. The cell proliferation has been regulated by diverse growth factors. Among them, insulin like growth factors(IGFs) are also involved in the pathogenesis of diabetic nephropathy. However, it is not yet known about the effect of high glucose on IGF-I and IGF-II secretion and the relationship between high glucose-induced secretion of IGFs and PKC or oxidative stress in the mesangial cells. Thus, we examined the mechanisms by which high glucose regulates secretion of IGFs in mesangial cells. High glucose(25 mM) increased IGF-I and IGF-II secretion. High glucose-induced increase of IGF-I and IGF-II secretion were blocked by taurine($2{\times}10^{-3}$ M), N-acetyl cystein(NAC, $10^{-5}M$), or GSH($10^{-5}M$) (antioxidants), suggesting the role of oxidative stress. High glucose-induced secretion of IGF-I and IGF-II were blocked by H-7, staurosporine, and bisindolylmaleimide I(protein kinase C inhibitors). On the other hand, high glucose also increased lipid peroxide (LPO) formation in a dose dependent manner. In addition, high glucoseinduced stimulation of LPO formation was blocked by PKC inhibitors. These results suggest that PKC is responsible for the increase of oxidative stress in the action of high glucose-induced secretion of IGF-I and IGF-II in mesangial cells. In conclusion, high glucose stimulates IGF-I and IGF-II secretion via PKCoxidative stress signal pathways in mesangial cells.

• Proceedings of the Korean Society of Plant Biotechnology Conference
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• 2004.10a
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• pp.208-208
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• 2004

• BMB Reports
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• v.48 no.3
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• pp.184-189
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• 2015

Src homology 2-containing protein tyrosine phosphatase 2 (SHP-2) is known to protect neurons from neurodegeneration during ischemia/reperfusion injury. We recently reported that ROS-mediated oxidative stress promotes phosphorylation of endogenous SHP-2 in astrocytes and complex formation between caveolin-1 and SHP-2 in response to oxidative stress. To examine the region of SHP-2 participating in complex formation with caveolin-1, we generated three deletion mutant constructs and six point mutation constructs of SHP-2. Compared with wild-type SHP-2, binding of the N-SH2 domain deletion mutant of SHP-2 to p-caveolin-1 was reduced greatly, using flow cytometric competitive binding assays and surface plasmon resonance (SPR). Moreover, deletion of the N-SH2 domain of SHP-2 affected $H_2O_2$-mediated ERK phosphorylation and Src phosphorylation at Tyr 419 in primary astrocytes, suggesting that N-SH2 domain of SHP-2 is responsible for the binding of caveolin-1 and contributes to the regulation of Src phosphorylation and activation following ROS-induced oxidative stress in brain astrocytes.

• Clinical and Experimental Reproductive Medicine
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• v.48 no.2
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• pp.150-155
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• 2021

Objective: Oxidative stress (OS) plays a key role in the etiology of unexplained male infertility. Coenzyme Q10 (CoQ10) is a potent antioxidant that may improve semen quality and OS in infertile men with idiopathic oligoasthenoteratospermia (OAT), but the underlying mechanism is unknown. Therefore, the present study was undertaken to investigate the effect of CoQ10 on OS markers and sperm DNA damage in infertile patients with idiopathic OAT. Methods: This prospective controlled study included 50 patients with idiopathic OAT and 50 fertile men who served as controls. All patients underwent a comprehensive medical assessment. Patients and controls received 200 mg of oral CoQ10 once daily for 3 months. Semen and blood were collected and analyzed for sperm parameters, seminal CoQ10 levels, reactive oxygen species (ROS) levels, total antioxidant capacity, catalase, sperm DNA fragmentation (SDF), and serum hormonal profile. Results: The administration of CoQ10 to patients with idiopathic OAT significantly improved sperm quality and seminal antioxidant status and significantly reduced total ROS and SDF levels compared to pretreatment values. Conclusion: CoQ10, at a dose of 200 mg/day for 3 months, may be a potential therapy for infertile patients with idiopathic OAT, as it improved sperm parameters and reduced OS and SDF in these patients.

• Proceedings of the Zoological Society Korea Conference
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• 2003.08a
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• pp.193.3-193
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• 2003

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 2003.08a
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• pp.194.3-194
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• 2003

No Abstract, See Full Text

• Journal of Physiology & Pathology in Korean Medicine
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• v.35 no.5
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• pp.185-192
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• 2021

The purpose of this study is to identify the effects of lifestyle, study stress and training stress on health status, and provide fundamental data for health management of university students majoring in physical education. In this study, 149 students participated and they were surveyed demographic characteristics, lifestyle, Maslach burnout inventory (student stress inventory), training stress inventory, and Mibyeong index. Height and weight were measured for calculating BMI. For statistical analysis, Student t-test, ANOVA test, chi-square test, correlation analysis, and multinominal logistic regression test has been used. There were differences between Mibyeong groups according to digestion status, smoking for female students and quality of sleeping for both male and female students. Study stress and training stress also affected to health status. Cynicism among study stress categories and all categories among training stress showed differences between sex. Correlation analysis and logistics regression analysis was used to estimate related factors of health status after adjusting for sex and age. Based on logistics regression analysis, quality of sleeping affected to Mibyeong 1 group and quality of sleeping, smoking and digestion status affected to Mibyeong 2 group. Among training stress category, dissatisfaction with game result and skills and lack of leisure time were affected to both Mibyeong 1 and 2 group. This study suggests that lifestyle, study stress and training stress might be significantly associated with university students majoring in physical education. Through managing those influence factors, health status of students could be improved.

• Journal of Animal Science and Technology
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• v.63 no.3
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• pp.531-544
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• 2021

Heat stress (HS) damages health and decreases performance variables in pigs, and if severe enough, causes mortality. However, metabolic changes under HS and recovery following HS are poorly understood. Therefore, this study was aimed to expose the essential mechanisms by which growing pigs respond to HS and the temporal pattern of plasma concentrations (PC) of amino acids (AAs) and metabolites. Crossbred male growing pigs were penned separately and allowed to adapt to thermal-neutral (TN) conditions (20℃ and 80% relative humidity; TN[-1D]). On the first day, all pigs were exposed to HS for 24 h (36℃ and 60% relative humidity), then to TN conditions for 5 days (TN[2D] to TN[5D]). All pigs had ad libitum access to water and 3 kg feed twice daily. Rectal temperature (RT) and feed intake (FI) were determined daily. HS pigs had higher RT (40.72℃) and lower (50%) FI than TN(-1D) pigs (p < 0.01). The PC of indispensable (threonine, valine, and methionine) and dispensable (cysteine and tyrosine) AAs were higher (p < 0.05) in HS than TN(-1D) pigs and remained increased during recovery time. Nonprotein α-aminobutyric acid and β-alanine concentrations were higher (p < 0.05) in HS than TN(-1D) pigs. The metabolite concentration of creatinine was higher (p < 0.01) under HS treatment than other treatments, but that of alanine and leucine remained increased (p < 0.05) through 5 d of recovery. In summary, some major differences were found in plasma AA profiles and metabolites between HS- and TN-condition pigs. This indicates that the HS pigs were forced to alter their metabolism, and these results provide information about mechanisms of acute HS responses relative to the recovery time.

• Molecules and Cells
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• v.47 no.1
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• pp.100006.1-100006.10
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• 2024

Nitric oxide (NO) serves as an evolutionarily conserved signaling molecule that plays an important role in a wide variety of cellular processes. Extensive studies in Drosophila melanogaster have revealed that NO signaling is required for development, physiology, and stress responses in many different types of cells. In neuronal cells, multiple NO signaling pathways appear to operate in different combinations to regulate learning and memory formation, synaptic transmission, selective synaptic connections, axon degeneration, and axon regrowth. During organ development, elevated NO signaling suppresses cell cycle progression, whereas downregulated NO leads to an increase in larval body size via modulation of hormone signaling. The most striking feature of the Drosophila NO synthase is that various stressors, such as neuropeptides, aberrant proteins, hypoxia, bacterial infection, and mechanical injury, can activate Drosophila NO synthase, initially regulating cellular physiology to enable cells to survive. However, under severe stress or pathophysiological conditions, high levels of NO promote regulated cell death and the development of neurodegenerative diseases. In this review, I highlight and discuss the current understanding of molecular mechanisms by which NO signaling regulates distinct cellular functions and behaviors.