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Article: Physical and Physiological Predictors Determining the Maximal Static Apnea Diving Time of Male Freedivers.

Lee, Dai-Woo / Yang, Hongwei / Ju, Jeong-Sun

Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc

2024 Volume 51, Issue 1, Page(s) 85–92

Abstract: This study aimed to investigate what factors determine freedivers' maximal static apnea dive time. We correlated some physical/physiological factors with male freedivers' maximum apnea diving duration. Thirty-six experienced male freedivers participated ... ...

Abstract	This study aimed to investigate what factors determine freedivers' maximal static apnea dive time. We correlated some physical/physiological factors with male freedivers' maximum apnea diving duration. Thirty-six experienced male freedivers participated in this study. The divers participated in two days of the experiments. On the first day, apnea diving time, blood oxygen saturation (SpO
MeSH term(s)	Humans ; Apnea/etiology ; Diving ; 3-Hydroxybutyric Acid ; Blood Glucose ; Lactic Acid
Chemical Substances	3-Hydroxybutyric Acid (TZP1275679) ; Blood Glucose ; Lactic Acid (33X04XA5AT)
Language	English
Publishing date	2024-04-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	1154414-4
ISSN	1066-2936
ISSN	1066-2936
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Article: The effects of heliox non-saturation diving on the cardiovascular system and cognitive functions.

Lee, Dal-Woo / Jung, Su-Jeen / Ju, Jeong-Sun

Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc

2020 Volume 47, Issue 1, Page(s) 93–100

Abstract: The purpose of this study was to investigate the effects of a single bout of heliox non-saturation diving on the cardiovascular system and cognitive function. Ten recreational scuba divers (10 males, ∼35 years old) participated in this study. These ... ...

Abstract	The purpose of this study was to investigate the effects of a single bout of heliox non-saturation diving on the cardiovascular system and cognitive function. Ten recreational scuba divers (10 males, ∼35 years old) participated in this study. These subjects made two pool dives within a one-week interval, alternating gases with compressed air (21% O2, 79% N2) and with heliox (21% O2 and 79% He). The depth was to 26 meters over a 20-minute duration. The results showed that heliox diving significantly increased blood O2 saturation by 1.15% and significantly decreased blood lactate levels by ∼57% when compared with air diving (P ≺ 0.05). However, there were no significant differences in resting heart rate, systolic or diastolic pressure, core body blood pressure, and pulse wave velocity between the heliox and air dives. The Stroop test showed that the heliox dive significantly increased cognitive function compared with the air dive in both the simple test (Offtime) and interference test (Ontime) (P ≺ 0.05). It was concluded that the heliox dive increases blood O2 saturation and decreases blood lactate concentration when compared with air dives. These conditions are likely to help divers reduce hypoxia in the water, reduce the risk of loss of consciousness, reduce fatigue and allow them to dive for longer. Heliox diving may also help judgment and risk coping skills in the water due to the improvement of cognitive ability as compared to air breathing dives.
MeSH term(s)	Adult ; Air ; Blood Pressure/drug effects ; Cardiovascular System/drug effects ; Cell Hypoxia ; Cognition/drug effects ; Diving/physiology ; Heart Rate/drug effects ; Helium/pharmacology ; Humans ; Hypoxia/blood ; Hypoxia/prevention & control ; Lactic Acid/blood ; Male ; Oxygen/blood ; Oxygen/pharmacology ; Pulse Wave Analysis ; Recreation ; Time Factors ; Vascular Stiffness
Chemical Substances	Helium (206GF3GB41) ; Lactic Acid (33X04XA5AT) ; heliox (58933-55-4) ; Oxygen (S88TT14065)
Language	English
Publishing date	2020-03-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1154414-4
ISSN	1066-2936
ISSN	1066-2936
DOI	10.22462/01.03.2020.10
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Article: Measurement of autophagy flux in benign prostatic hyperplasia in vitro.

Oh, Sung-Hee / Lee, Dong-Won / Choi, Yong-Bok / Lee, Yoo-Hyun / Ju, Jeong-Sun

Prostate international

2020 Volume 8, Issue 2, Page(s) 70–77

Abstract: Background: Recent studies have suggested a novel therapeutic strategy for treatment of benign prostatic hyperplasia (BPH) via modulation of autophagy. However, it is not clear whether autophagy induction or inhibition can render better therapeutic ... ...

Abstract	Background: Recent studies have suggested a novel therapeutic strategy for treatment of benign prostatic hyperplasia (BPH) via modulation of autophagy. However, it is not clear whether autophagy induction or inhibition can render better therapeutic efficacy for BPH treatment because autophagy activation in BPH tissue is not precisely known and still contradictory. The purpose of this study was to examine the levels of autophagy in BPH tissue cells. Methods: We have analyzed and compared autophagic flux which is defined as a measure of autophagic degradation activity in two human prostate epithelial cell lines, RWPE-1 (normal prostate) and BPH-1 (BPH) using LC3-II turnover assay, to clarify the levels of autophagy in BPH. Results: The Conclusion: It is suggested that defective autophagy, which is decreased autophagy flux in the prostate gland, may be implicated in BPH, and activating autophagy flux of the prostate with BPH may be used as a potential therapeutic target for treating and alleviating BPH disease.
Language	English
Publishing date	2020-02-26
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2711928-2
ISSN	2287-903X ; 2287-8882
ISSN (online)	2287-903X
ISSN	2287-8882
DOI	10.1016/j.prnil.2019.11.004
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Article ; Online: Inclusion body myopathy, Paget's disease of the bone and fronto-temporal dementia: a disorder of autophagy.

Ju, Jeong-Sun / Weihl, Conrad C

Human molecular genetics

2010 Volume 19, Issue R1, Page(s) R38–45

Abstract: Inclusion body myopathy associated with Paget's disease of the bone and fronto-temporal dementia (IBMPFD) is a progressive autosomal dominant disorder caused by mutations in p97/VCP (valosin-containing protein). p97/VCP is a member of the AAA+ (ATPase ... ...

Abstract	Inclusion body myopathy associated with Paget's disease of the bone and fronto-temporal dementia (IBMPFD) is a progressive autosomal dominant disorder caused by mutations in p97/VCP (valosin-containing protein). p97/VCP is a member of the AAA+ (ATPase associated with a variety of activities) protein family and participates in multiple cellular processes. One particularly important role for p97/VCP is facilitating intracellular protein degradation. p97/VCP has traditionally been thought to mediate the ubiquitin-proteasome degradation of proteins; however, recent studies challenge this dogma. p97/VCP clearly participates in the degradation of aggregate-prone proteins, a process principally mediated by autophagy. In addition, IBMPFD mutations in p97/VCP lead to accumulation of autophagic structures in patient and transgenic animal tissue. This is likely due to a defect in p97/VCP-mediated autophagosome maturation. The following review will discuss the evidence for p97/VCP in autophagy and how a disruption in this process contributes to IBMPFD pathogenesis.
MeSH term(s)	Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/physiology ; Autophagy ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/physiology ; Frontotemporal Dementia/complications ; Frontotemporal Dementia/genetics ; Homeostasis ; Humans ; Mutation ; Myositis, Inclusion Body/complications ; Myositis, Inclusion Body/genetics ; Osteitis Deformans/complications ; Osteitis Deformans/genetics ; Valosin Containing Protein
Chemical Substances	Cell Cycle Proteins ; Adenosine Triphosphatases (EC 3.6.1.-) ; VCP protein, human (EC 3.6.4.6) ; Valosin Containing Protein (EC 3.6.4.6)
Language	English
Publishing date	2010-04-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddq157
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Article ; Online: p97/VCP at the intersection of the autophagy and the ubiquitin proteasome system.

Ju, Jeong-Sun / Weihl, Conrad C

Autophagy

2010 Volume 6, Issue 2, Page(s) 283–285

MeSH term(s)	Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/metabolism ; Animals ; Autophagy/physiology ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/pathology ; Frontotemporal Dementia/physiopathology ; Humans ; Mice ; Myositis, Inclusion Body/genetics ; Myositis, Inclusion Body/pathology ; Myositis, Inclusion Body/physiopathology ; Osteitis Deformans/genetics ; Osteitis Deformans/pathology ; Osteitis Deformans/physiopathology ; Proteasome Endopeptidase Complex/metabolism ; Ubiquitin/metabolism ; Valosin Containing Protein
Chemical Substances	Cell Cycle Proteins ; Ubiquitin ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Adenosine Triphosphatases (EC 3.6.1.-) ; VCP protein, human (EC 3.6.4.6) ; Valosin Containing Protein (EC 3.6.4.6) ; Vcp protein, mouse (EC 3.6.4.6)
Language	English
Publishing date	2010-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.6.2.11063
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Article: Comparisons of ELISA and Western blot assays for detection of autophagy flux.

Oh, Sung-Hee / Choi, Yong-Bok / Kim, June-Hyun / Weihl, Conrad C / Ju, Jeong-Sun

Data in brief

2017 Volume 13, Page(s) 696–699

Abstract: We analyzed autophagy/mitophagy ... ...

Abstract	We analyzed autophagy/mitophagy flux
Language	English
Publishing date	2017-07-04
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2017.06.045
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Article ; Online: Quantification of autophagy flux using LC3 ELISA.

Oh, Sung-Hee / Choi, Yong-Bok / Kim, June-Hyun / Weihl, Conrad C / Ju, Jeong-Sun

Analytical biochemistry

2017 Volume 530, Page(s) 57–67

Abstract: Macroautophagy (hereafter referred to as autophagy) is a degradation system that delivers cytoplasmic materials to lysosomes via autophagosomes. Autophagic flux is defined as a measure of autophagic degradation activity. Despite several methods for ... ...

Abstract	Macroautophagy (hereafter referred to as autophagy) is a degradation system that delivers cytoplasmic materials to lysosomes via autophagosomes. Autophagic flux is defined as a measure of autophagic degradation activity. Despite several methods for monitoring autophagic flux being currently utilized, interest in finding a highly accurate, sensitive and well-quantifiable assay is still growing. Therefore, we introduce a new approach analyzing autophagic flux in vitro and in vivo using enzyme-linked immunosorbent assay (ELISA) technique. In order to adapt this assay from LC3-II turnover measured by Western blot in the presence and absence of lysosomal inhibitors, we induced autophagy by starvation or rapamycin and mitophagy (mitochondrial degradation by autophagy) by CCCP in C2C12 myotubes for 8 h and in mice for 48 h with and without Bafilomycin A1 or colchicine treatment, respectively. Following subcellular fractionation of mouse skeletal muscle cells and tissue, cytosolic, membrane, and mitochondrial fractions were analyzed through a sandwich ELISA using two LC3 antibodies, LC3 capture and HRP-conjugated LC3 detection antibodies. Using this ELISA, changes in the membrane-bound or mitochondrion-associated LC3-II levels, and the ratio of the LC3-II from each fraction to LC3-I levels (cytosolic fraction) were evaluated for measuring autophagy and mitophagy flux. This study demonstrates that this ELISA was more sensitive and reliable to measure autophagic/mitophagic flux in both in vitro and in vivo, compared with the most commonly used LC3 turnover assay via Western blot.
MeSH term(s)	Animals ; Autophagy ; Blotting, Western ; Cell Compartmentation ; Cells, Cultured ; Enzyme-Linked Immunosorbent Assay/methods ; Lysosomes/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/metabolism ; Mitochondria/metabolism ; Mitochondria/pathology ; Muscle Fibers, Skeletal/metabolism ; Muscle Fibers, Skeletal/pathology ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology
Chemical Substances	Map1lc3b protein, mouse ; Microtubule-Associated Proteins
Language	English
Publishing date	2017-05-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1110-1
ISSN	1096-0309 ; 0003-2697
ISSN (online)	1096-0309
ISSN	0003-2697
DOI	10.1016/j.ab.2017.05.003
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Article: Comparisons of ELISA and Western blot assays for detection of autophagy flux

Oh, Sung-hee / Choi, Yong-bok / Kim, June-hyun / Weihl, Conrad C. / Ju, Jeong-sun

Data in Brief. 2017 Aug., v. 13

2017

Abstract: We analyzed autophagy/mitophagy flux in vitro (C2C12 myotubes) and in vivo (mouse skeletal muscle) following the treatments of autophagy inducers (starvation, rapamycin) and a mitophagy inducer (carbonyl cyanide m-chlorophenylhydrazone, CCCP) using two ... ...

Abstract	We analyzed autophagy/mitophagy flux in vitro (C2C12 myotubes) and in vivo (mouse skeletal muscle) following the treatments of autophagy inducers (starvation, rapamycin) and a mitophagy inducer (carbonyl cyanide m-chlorophenylhydrazone, CCCP) using two immunodetection methods, ELISA and Western blotting, and compared their working range, accuracy, and reliability. The ELISAs showed a broader working range than that of the LC3 Western blots (Table 1). Table 2 showed that data value distribution was tighter and the average standard error from the ELISA was much smaller than those of the Western blot, directly relating to the accuracy of the assay. Test-retest reliability analysis showed good reliability for three individual ELISAs (interclass correlation, ≥ 0.7), but poor reliability for three individual Western blots (interclass correlation, ≤ 0.4) (Table 3).
Keywords	Western blotting ; cyanides ; mice ; mitophagy ; myotubes ; rapamycin ; skeletal muscle ; starvation
Language	English
Dates of publication	2017-08
Size	p. 696-699.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2017.06.045
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Article ; Online: Autophagy plays a role in skeletal muscle mitochondrial biogenesis in an endurance exercise-trained condition.

Ju, Jeong-Sun / Jeon, Sei-Il / Park, Je-Young / Lee, Jong-Young / Lee, Seong-Cheol / Cho, Ki-Jung / Jeong, Jong-Moon

The journal of physiological sciences : JPS

2016 Volume 66, Issue 5, Page(s) 417–430

Abstract: Mitochondrial homeostasis is tightly regulated by two major processes: mitochondrial biogenesis and mitochondrial degradation by autophagy (mitophagy). Research in mitochondrial biogenesis in skeletal muscle in response to endurance exercise training has ...

Abstract	Mitochondrial homeostasis is tightly regulated by two major processes: mitochondrial biogenesis and mitochondrial degradation by autophagy (mitophagy). Research in mitochondrial biogenesis in skeletal muscle in response to endurance exercise training has been well established, while the mechanisms regulating mitophagy and the interplay between mitochondrial biogenesis and degradation following endurance exercise training are not yet well defined. The purpose of this study was to examine the effects of a short-term inhibition of autophagy in response to acute endurance exercise on skeletal muscle mitochondrial biogenesis and dynamics in an exercise-trained condition. Male wild-type C57BL/6 mice performed five daily bouts of 1-h swimming per week for 8 weeks. In order to measure autophagy flux in mouse skeletal muscle, mice were treated with or without 2 days of 0.4 mg/kg/day intraperitoneal colchicine (blocking the degradation of autophagosomes) following swimming exercise training. The autophagic flux assay demonstrated that swimming training resulted in an increase in the autophagic flux (~100 % increase in LC3-II) in mouse skeletal muscle. Mitochondrial fusion proteins, Opa1 and MFN2, were significantly elevated, and mitochondrial fission protein, Drp1, was also increased in trained mouse skeletal muscle, suggesting that endurance exercise training promotes both mitochondrial fusion and fission processes. A mitochondrial receptor, Bnip3, was further increased in exercised muscle when treated with colchicine while Pink/Parkin protein levels were unchanged. The endurance exercise training induced increases in mitochondrial biogenesis marker proteins, SDH, COX IV, and a mitochondrial biogenesis promoting factor, PGC-1α but this effect was abolished in colchicine-treated mouse skeletal muscle. This suggests that autophagy plays an important role in mitochondrial biogenesis and this coordination between these opposing processes is involved in the cellular adaptation to endurance exercise training.
MeSH term(s)	Animals ; Autophagy/physiology ; Colchicine/pharmacology ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Muscle, Skeletal/metabolism ; Organelle Biogenesis ; Physical Conditioning, Animal/physiology ; Physical Endurance/physiology ; Swimming/physiology
Chemical Substances	BNip3 protein, mouse ; Membrane Proteins ; Mitochondrial Proteins ; GTP Phosphohydrolases (EC 3.6.1.-) ; Mfn2 protein, mouse (EC 3.6.1.-) ; Opa1 protein, mouse (EC 3.6.1.-) ; Colchicine (SML2Y3J35T)
Language	English
Publishing date	2016-03-04
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2234472-X
ISSN	1880-6562 ; 1880-6546
ISSN (online)	1880-6562
ISSN	1880-6546
DOI	10.1007/s12576-016-0440-9
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Article ; Online: Increased autophagy accelerates colchicine-induced muscle toxicity.

Ching, James K / Ju, Jeong Sun / Pittman, Sara K / Margeta, Marta / Weihl, Conrad C

Autophagy

2013 Volume 9, Issue 12, Page(s) 2115–2125

Abstract: Colchicine treatment is associated with an autophagic vacuolar myopathy in human patients. The presumed mechanism of colchicine-induced myotoxicity is the destabilization of the microtubule system that leads to impaired autophagosome-lysosome fusion and ... ...

Abstract	Colchicine treatment is associated with an autophagic vacuolar myopathy in human patients. The presumed mechanism of colchicine-induced myotoxicity is the destabilization of the microtubule system that leads to impaired autophagosome-lysosome fusion and the accumulation of autophagic vacuoles. Using the MTOR inhibitor rapamycin we augmented colchicine’s myotoxic effect by increasing the autophagic flux; this resulted in an acute myopathy with muscle necrosis. In contrast to myonecrosis induced by cardiotoxin, myonecrosis induced by a combination of rapamycin and colchicine was associated with accumulation of autophagic substrates such as LC3-II and SQSTM1; as a result, autophagic vacuoles accumulated in the center of myofibers, where LC3-positive autophagosomes failed to colocalize with the lysosomal protein marker LAMP2. A similar pattern of central LC3 accumulation and myonecrosis is seen in human patients with colchicine myopathy, many of whom have been treated with statins (HMGCR/HMG-CoA reductase inhibitors) in addition to colchicine. In mice, cotreatment with colchicine and simvastatin also led to muscle necrosis and LC3 accumulation, suggesting that, like rapamycin, simvastatin activates autophagy. Consistent with this, treatment of mice with four different statin medications enhanced autophagic flux in skeletal muscle in vivo. Polypharmacy is a known risk factor for toxic myopathies; our data suggest that some medication combinations may simultaneously activate upstream autophagy signaling pathways while inhibiting the degradation of these newly synthesized autophagosomes, resulting in myotoxicity.
MeSH term(s)	Animals ; Autophagy/drug effects ; Autophagy/physiology ; Colchicine/pharmacology ; Disease Progression ; Humans ; Lysosomal Storage Diseases/chemically induced ; Lysosomal Storage Diseases/pathology ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/pathology ; Muscle, Skeletal/physiopathology ; Muscular Diseases/chemically induced ; Muscular Diseases/pathology ; Phagosomes/drug effects ; Phagosomes/pathology ; Simvastatin/pharmacology ; Up-Regulation/drug effects ; Vacuoles/drug effects ; Vacuoles/pathology
Chemical Substances	Simvastatin (AGG2FN16EV) ; Colchicine (SML2Y3J35T)
Language	English
Publishing date	2013-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.26150
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