• Molecules and Cells
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• v.46 no.11
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• pp.655-663
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• 2023

Autophagy dysfunction is associated with human diseases and conditions including neurodegenerative diseases, metabolic issues, and chronic infections. Additionally, the decline in autophagic activity contributes to tissue and organ dysfunction and aging-related diseases. Several factors, such as down-regulation of autophagy components and activators, oxidative damage, microinflammation, and impaired autophagy flux, are linked to autophagy decline. An autophagy flux impairment (AFI) has been implicated in neurological disorders and in certain other pathological conditions. Here, to enhance our understanding of AFI, we conducted a comprehensive literature review of findings derived from two well-studied cellular stress models: glucose deprivation and replicative senescence. Glucose deprivation is a condition in which cells heavily rely on oxidative phosphorylation for ATP generation. Autophagy is activated, but its flux is hindered at the autolysis step, primarily due to an impairment of lysosomal acidity. Cells undergoing replicative senescence also experience AFI, which is also known to be caused by lysosomal acidity failure. Both glucose deprivation and replicative senescence elevate levels of reactive oxygen species (ROS), affecting lysosomal acidification. Mitochondrial alterations play a crucial role in elevating ROS generation and reducing lysosomal acidity, highlighting their association with autophagy dysfunction and disease conditions. This paper delves into the underlying molecular and cellular pathways of AFI in glucose-deprived cells, providing insights into potential strategies for managing AFI that is driven by lysosomal acidity failure. Furthermore, the investigation on the roles of mitochondrial dysfunction sheds light on the potential effectiveness of modulating mitochondrial function to overcome AFI, offering new possibilities for therapeutic interventions.

• Korean Journal of Biological Psychiatry
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• v.13 no.1
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• pp.38-42
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• 2006

The case of a 66- year-old woman with coexisting idiopathic basal ganglia calcification(IBGC) and dementia was presented. The calcification was detected in bilateral basal ganglia, dentate nucleus, and thalamus by brain imaging. Serum calcium and phosphorus levels were normal. The underlying diseases of calcification of basal ganglia such as parathyroid dysfunction and other infectious, toxic, or metabolic illness were excluded. The patient had memory impairment and frontal executive dysfunction without aphasia, agnosia, apraxia, and visuospatial impairment in neuropsychological test. It suggested that the cognitive impairment might be due to the dysfunction of frontal-subcortical circuit.

• Child Health Nursing Research
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• v.1 no.1
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• pp.26-36
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• 1995

Children with metabolic disorders suffer from retardation and cognitive dysfunction. The task of caring for a mother may mean that she has less time and mony and more workload which may result in increased fatigue and depression and low well-being. The burden carried by mother due to the responsiblity take care of child. The descriptive study was done identify the burden in mother of children with metabolic disorders. The data was collected from November 1 to November 16, 1993. nineteen mothers were interviewed with metabolic disorders with questionnaire by mail. Burden was measured using existing tools by Zarit (1980), Montgomery(1985) . et al. Burden data was analyzed by the SPSS /pc+ program were tested using means, frequencies, Mann-Whitney, U-Wilcoxon Rank Sum Test and Kruskal-Wallis one way ANOVA The result of this study as follows : The meas score for burden was 2.8. (range from 34 to 4.95) The result of reiationship of demographic character and burden was no significant. In conclusion it was found that burden is correlated negatively to quality of life. In this study, burden was scored relatively low. Further qualitative research is needed to validats the nature of burden.

• BMB Reports
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• v.47 no.11
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• pp.599-608
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• 2014

As the prevalence of obesity has increased explosively over the last several decades, associated metabolic disorders, including type 2 diabetes, dyslipidemia, hypertension, and cardiovascular diseases, have been also increased. Thus, new strategies for preventing and treating them are needed. The nuclear peroxisome proliferator-activated receptors (PPARs) are involved fundamentally in regulating energy homeostasis; thus, they have been considered attractive drug targets for addressing metabolic disorders. Among the PPARs, $PPAR{\gamma}$ is a master regulator of gene expression for metabolism, inflammation, and other pathways in many cell types, especially adipocytes. It is a physiological receptor of the potent anti-diabetic drugs of the thiazolidinediones (TZDs) class, including rosiglitazone (Avandia). However, TZDs have undesirable and severe side effects, such as weight gain, fluid retention, and cardiovascular dysfunction. Recently, many reports have suggested that $PPAR{\gamma}$ could be modulated by post-translational modifications (PTMs), and modulation of PTM has been considered as novel approaches for treating metabolic disorders with fewer side effects than the TZDs. In this review, we discuss how PTM of $PPAR{\gamma}$ may be regulated and issues to be considered in making novel anti-diabetic drugs that can modulate the PTM of $PPAR{\gamma}$.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.25-28
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• 2015

Mitochondrial disorders are rare metabolic diseases. They often present during neonatal period but with nonspecific clinical features such as feeding difficulties, failure to thrive, and seizures. Mitochondrial defects have also known to be associated with neurological disorders, as well as cancers. We report the first case of neonatal mitochondrial respiratory chain defect with sarcoma botryoides confirmed by pathologic diagnosis, suggesting another possible link between mitochondrial dysfunction and cancer.

• Clinical and Experimental Reproductive Medicine
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• v.50 no.1
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• pp.1-11
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• 2023

In reproduction, mitochondria produce bioenergy, help to synthesize biomolecules, and support the ovaries, oogenesis, and preimplantation embryos, thereby facilitating healthy live births. However, the regulatory mechanism of mitochondria in oocytes and embryos during oogenesis and embryo development has not been clearly elucidated. The functional activity of mitochondria is crucial for determining the quality of oocytes and embryos; therefore, the underlying mechanism must be better understood. In this review, we summarize the specific role of mitochondria in reproduction in oocytes and embryos. We also briefly discuss the recovery of mitochondrial function in gametes and zygotes. First, we introduce the general characteristics of mitochondria in cells, including their roles in adenosine triphosphate and reactive oxygen species production, calcium homeostasis, and programmed cell death. Second, we present the unique characteristics of mitochondria in female reproduction, covering the bottleneck theory, mitochondrial shape, and mitochondrial metabolic pathways during oogenesis and preimplantation embryo development. Mitochondrial dysfunction is associated with ovarian aging, a diminished ovarian reserve, a poor ovarian response, and several reproduction problems in gametes and zygotes, such as aneuploidy and genetic disorders. Finally, we briefly describe which factors are involved in mitochondrial dysfunction and how mitochondrial function can be recovered in reproduction. We hope to provide a new viewpoint regarding factors that can overcome mitochondrial dysfunction in the field of reproductive medicine.

• BMB Reports
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• v.48 no.10
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• pp.571-576
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• 2015

SB743921 is a potent inhibitor of the spindle protein kinesin and is being investigated in ongoing clinical trials for the treatment of myeloma. However, little is known about the molecular events underlying the induction of cell death in multiple myeloma (MM) by SB743921, alone or in combination treatment. Here, we report that SB743921 induces mitochondria-mediated cell death via inhibition of the $NF-{\kappa}B$ signaling pathway, but does not cause cell cycle arrest in KMS20 MM cells. SB743921-mediated inhibition of the $NF-{\kappa}B$ pathway results in reduced expression of SOD2 and Mcl-1, leading to mitochondrial dysfunction. We also found that combination treatment with SB743921 and bortezomib induces death in bortezomib-resistant KMS20 cells. Altogether, these data suggest that treatment with SB743921 alone or in combination with bortezomib offers excellent translational potential and promises to be a novel MM therapy.

• Journal of Ginseng Research
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• v.43 no.3
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• pp.431-441
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• 2019

Background: The efficacy of ginseng, the representative product of Korea, and its chemical effects have been well investigated. The ginsenoside RG3 has been reported to exhibit apoptotic, anticancer, and antidepressant-like effects. Methods: In this report, the putative effect of RG3 on several cellular function including cell survival, differentiation, development and aging process were evaluated by monitoring each specific marker. Also, mitochondrial morphology and function were investigated in ultraviolet (UV)-irradiated normal human dermal fibroblast cells. Results: RG3 treatment increased the expression of extracellular matrix proteins, growth-associated immediate-early genes, and cell proliferation genes in UV-irradiated normal human dermal fibroblast cells. And, RG3 also resulted in enhanced expression of antioxidant proteins such as nuclear factor erythroid 2-related factor-2 and heme oxygenase-1. In addition, RG3 affects the morphology of UV-induced mitochondria and plays a role in protecting mitochondrial dysfunction. Conclusioin: RG3 restores mitochondrial adenosine triphosphate (ATP) and membrane potential via its antioxidant effects in skin cells damaged by UV irradiation, leading to an increase in proteins linked with the extracellular matrix, cell proliferation, and antioxidant activity.

• Journal of the Korean Magnetic Resonance Society
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• v.5 no.1
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• pp.56-65
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• 2001

Localized in vivo proton magnetic resonance spectroscopy (MRS) was performed to evaluate metabolic alterations in the right and left frontal lobe before and after neuroleptic treatment of schizophrenic patients (n=24) and a group of healthy normal subjects (n=20). Proton metabolic ratios obtained from the 8㎤ yokels in the right and left frontal lobe were compared with the clinical assessment of PANSS for each subject. There was no significant difference in the metabolic ratios between the right and the left frontal lobes in either the schizophrenic group or the control group, indicating no laterality. Compared with those of the normal control group, NAA/Cr and (GABA+Glu)/Cr ratios of the schizophrenic patients showed significantly lower (p=0.023) and higher (p=0.005) value, respectively. The (GABA+Glu)/Cr ratio of the schizophrenic patients was generally decreased after neuroleptic treatment, while the NAA/Cr ratio was not changed. Significant correlation between the (GABA+Glu)/Cr ratio and the clinical symptom scores assessed by PANSS was established. The present study supports the “hypofrontality” hypothesis of schizophrenia on the basis of the altered metabolic ratios before and after neuroleptic treatment.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.19 no.1
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• pp.30-38
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• 2009

The objective of this study was to evaluate the effects of occupational exposure to styrene on the components of metabolic syndrome. We surveyed 263 employees, among whom 117workers we ere chronically exposed to styrene in glass-reinforced plastic boat manufacturing factories and 146 controls had never been occupationally exposed to styrene as will as hazardous chemicals. The general and job characteristics such as age, smoking and drinking habit, working hours and duration were not significant different except sleeping hours(p<0.05). Among the components of metabolic syndrome, the systolic blood pressure, total cholesterol, HDL-cholesterol and fasting glucose were significantly higher in exposed workers. On multiple logistic regression analysis for the components of metabolic syndrome, waist circumference was insulin (OR=1.129), blood pressure was MA(OR=14.724), fasting glucose(OR=1.191) and metabolic syndrome(OR=1.110) were significantly associated with insulin. The mean concentration of airborne styrene was $ 38.1{\pm}40.1$ ppm, blood concentrations of glucose and insulin and levels of HOMA-IR in over 50 ppm exposed group were higher than in blow 50 ppm exposed group. These results suggested that the exposure of styrene affects blood pressure, fasting glucose and insulin levels and that dysfunction and/or declination in glucose and insulin metabolism might induced ultimately insulin resistance and metabolic syndrome.