16 results on '"Patcharee Kooncumchoo"'
Search Results
2. Acute effects of air pollution on all-cause mortality: a natural experiment from haze control measures in Chiang Mai Province, Thailand
- Author
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Nitaya Vajanapoom, Patcharee Kooncumchoo, and Thuan-Quoc Thach
- Subjects
Haze smoke ,Biomass burning ,Air pollution ,Particulate matter ,Mortality ,Health effects ,Medicine ,Biology (General) ,QH301-705.5 - Abstract
Background Serious haze episodes have been a seasonal event in Chiang Mai province for more than a decade. In 2008, local government agencies introduced comprehensive measures to control haze and limit its impacts on public health. This study assessed the acute effects of ambient air pollutants on all-cause mortality before and after the introduction of those haze control measures. Methods We obtained daily mortality counts and data on mass concentrations of particulate matter
- Published
- 2020
- Full Text
- View/download PDF
3. Locomotor Recovery Following 8 Weeks of I-Walk Gait Training in Subacute Stroke.
- Author
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Pakaon Saipan, Patcharee Kooncumchoo, Kornanong Yuenyongchaiwat, Bunyong Rungroungdouyboon, Pornpimol Muanjai, Oranat Sukkho, and Nongnuch Loungpon
- Subjects
FITNESS walking ,STROKE ,GAIT in humans ,STROKE patients ,CONTROL groups - Abstract
The custom-designed robotic gait aid "I-Walk" was developed to enhance ambulation and facilitate cost-effective repetitive training. However, empirical evidence regarding its impact on cardiovascular endurance remains scarce. This study assessed the beneficial effects of 8 weeks of I-Walk gait training on walking endurance and aerobic capacity in 11 subacute stroke patients 45 to 70 years of age within 6 months of their first stroke. They were randomly assigned to the Control Group (n = 5) and the I-Walk Gait Training Group (n = 6). All underwent a daily 60-min session, 3 d·wk
-1 for 8 wks. The program included a 30-min PT session, and 30 min of gait training (overground or using the I-Walk). Walking distance and aerobic capacity were measured using the 6 Minute Walk Test (6MWT) before and after the intervention. After the 8 weeks of I-Walk Gait Training, the average walking distance increased by 60 m (P = 0.039) with a mean peak VO2 increase of 1.38 ml·kg-1 ·min-1 (0.11-2.65 ml·kg-1 ·min-1 , P = 0.039) vs. an average increase of 44 m (P = 0.107) with overground training. The I-Walk with a conventional PT program increased the 6MWT performance in the subacute stroke patients with progressive improvement over the intervention period. [ABSTRACT FROM AUTHOR]- Published
- 2024
4. Lumbo-Pelvic-Hip Angle Changes During Upright and Free Style Sitting in Office Workers with Lower Crossed Syndrome.
- Author
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Pailin Puagprakong, Poramet Earde, and Patcharee Kooncumchoo
- Published
- 2021
- Full Text
- View/download PDF
5. Gait Improvement in Chronic Stroke Survivors by Using an Innovative Gait Training Machine: A Randomized Controlled Trial
- Author
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Patcharee Kooncumchoo, Phuwarin Namdaeng, Somrudee Hanmanop, Bunyong Rungroungdouyboon, Kultida Klarod, Sirirat Kiatkulanusorn, and Nongnuch Luangpon
- Subjects
Health, Toxicology and Mutagenesis ,Public Health, Environmental and Occupational Health ,Stroke Rehabilitation ,lower limb impairment ,stroke ,Article ,Exercise Therapy ,motor recovery ,Treatment Outcome ,gait training ,Humans ,Medicine ,Survivors ,Gait ,human activities - Abstract
Chronic stroke leads to the impairment of lower limb function and gait performance. After in-hospital rehabilitation, most individuals lack continuous gait training because of the limited number of physical therapists. This study aimed to evaluate the effects of a newly invented gait training machine (I-Walk) on lower limb function and gait performance in chronic stroke individuals. Thirty community-dwelling chronic stroke individuals were allocated to the I-Walk machine group (n = 15) or the overground gait training (control) group (n = 15). Both groups received 30 min of upper limb and hand movement and sit-to-stand training. After that, the I-Walk group received 30 min of I-Walk training, while the control followed a 30-minute overground training program. All the individuals were trained 3 days/week for 8 weeks. The primary outcome of the motor recovery of lower limb impairment was measured using the Fugl–Meyer Assessment (FMA). The secondary outcomes for gait performance were the 6-minute walk test (6 MWT), the 10-meter walk test (10 MWT), and the Timed Up and Go (TUG). The two-way mixed-model ANOVA with the Bonferroni test was used to compare means within and between groups. The post-intervention motor and sensory subscales of the FMA significantly increased compared to the baseline in both groups. Moreover, the 6 MWT and 10 MWT values also improved in both groups. In addition, the mean difference of TUG in the I-Walk was higher than the control. The efficiency of I-Walk training was comparable to overground training and might be applied for chronic stroke gait training in the community.
- Published
- 2022
6. Heart Rate Variability Response in Children Working at Height
- Author
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Patcharee Kooncumchoo
- Subjects
Work at height ,Heart rate variability (HRV) ,Children - Abstract
Science & Technology Asia, 25, 3, 29-37
- Published
- 2020
- Full Text
- View/download PDF
7. Effects of I-Walk Training on Gait Performances in Patients with Chronic Stroke
- Author
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Nathamon Pansuksawat, Noppol Pramodhyakul, Pinailug Tantilipikorn Earde, Patcharee Kooncumchoo, and Bunyong Rungroungdouyboon
- Subjects
Task-specific training ,Hemiplegia ,Gait training ,Physical therapy ,Robotic - Abstract
Vajira Medical Journal, 64, 4, 243-254
- Published
- 2020
- Full Text
- View/download PDF
8. Differences in Grip Strength amongWheelchair Basketball Athletes: Variationsby Hand Size and Handrim-Tire Diameter
- Author
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Patcharee Kooncumchoo
- Subjects
Handrim-tire distance ,Grip strength ,Hand size ,Handrim ,Wheelchair basketball - Abstract
Science & Technology Asia, 25, 3, 141-151
- Published
- 2020
- Full Text
- View/download PDF
9. D2-1 L4/L5 disc compression force in phases of manual human handling
- Author
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Chanya Jiemjai, Patcharee Kooncumchoo, Santhanee Khruakhorn, and Naris Charoenporn
- Subjects
business.industry ,Mechanical engineering ,Medicine ,business - Published
- 2017
10. Video-Based Postural Hazard Identification during Flood Victim Evacuation
- Author
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Teeraphun Kaewdok, Sasitorn Taptagaporn, Naris Charoenporn, Patcharee Kooncumchoo, and Pagamas Piriyaprasarth
- Subjects
Public health preparedness, Musculoskeletal injury, Emergency responder, Ergonomics, Flood - Abstract
1, 21, Thammasat International Journal of Science and Technology
- Published
- 2016
- Full Text
- View/download PDF
11. Salsolinol, an Endogenous Neurotoxin, Activates JNK and NF-κB Signaling Pathways in Human Neuroblastoma Cells
- Author
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Shaik Shavali, Piyarat Govitrapong, Manuchair Ebadi, Sawitri Wanpen, and Patcharee Kooncumchoo
- Subjects
Mitochondrion ,Biology ,medicine.disease_cause ,Biochemistry ,Neuroblastoma ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Cell Line, Tumor ,medicine ,Humans ,Neurotoxin ,Phosphorylation ,Electron Transport Complex I ,c-jun ,Dopaminergic ,JNK Mitogen-Activated Protein Kinases ,NF-kappa B ,Cytochromes c ,NF-κB ,General Medicine ,Isoquinolines ,Molecular biology ,Mitochondria ,Cell biology ,IκBα ,chemistry ,Signal transduction ,Reactive Oxygen Species ,Oxidative stress ,Signal Transduction - Abstract
Salsolinol, an endogenous neurotoxin, is known to be involved in the pathogenesis of Parkinson's disease (PD). In the present study, we have investigated the effects of salsolinol on the activation of two different signaling pathways that involve c-Jun N-terminal kinase (JNK), and nuclear factor-kappaB, (NF-kappaB) in human dopaminergic neuroblastoma SH-SY5Y cells. Salsolinol treatment caused upregulation in the levels of c-Jun and phosphorylated c-Jun. It also caused degradation of IkappaBalpha and translocated the active NF-kappaB into the nucleus. The binding activity of NF-kappaB to DNA was enhanced by salsolinol in a concentration dependent manner. Furthermore, salsolinol decreased the levels of the anti-apoptotic protein Bcl-2, and increased pro-apoptotic protein Bax, while enhancing the release of cytochrome-c from mitochondria. Mitochondrial complex-I activity was significantly decreased and reactive oxygen species (ROS) were increased in salsolinol treated cells. These results partly suggest that salsolinol-induced JNK and NF-kappaB signaling pathways may be involved in induction of apoptosis in human dopaminergic neurons, as seen in Parkinson's disease.
- Published
- 2007
12. Coenzyme Q10 Provides Neuroprotection in Iron-Induced Apoptosis in Dopaminergic Neurons
- Author
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James E. Porter, Sushil Sharma, Piyarat Govitrapong, Patcharee Kooncumchoo, and Manuchir Ebadi
- Subjects
Coenzyme Q10 ,medicine.medical_specialty ,Pars compacta ,MPTP ,Substantia nigra ,General Medicine ,Biology ,medicine.disease_cause ,Neuroprotection ,Ferritin ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Endocrinology ,chemistry ,Neuromelanin ,Internal medicine ,biology.protein ,medicine ,Oxidative stress - Abstract
The exact molecular mechanism of progressive loss of neuromelanin containing nigrostriatal dopaminergic neurons in Parkinson's disease (PD) remains unknown, yet evidence suggests that iron might play an important role in PD pathology. In this study we have determined the neuroprotective role of coenzyme Q(10) (CoQ(10)) in ironinduced apoptosis in cultured human dopaminergic (SK-N-SH) neurons, in metallothionein gene- manipulated mice, and in alpha-synuclein knockout (alpha-synko) mice with a primary objective to assess a possible therapeutic and anti-inflammatory potential for CoQ(10) in PD. Iron-induced mitochondrial damage and apoptosis were characterized by reactive oxygen species production, increased metallothionein and glutathione synthesis, caspase- 3 activation, NF-kappaB induction, and decreased Bcl-2 expression, without any significant change in Bax expression. Lower concentrations of FeSO4 (1-10 microM) induced perinuclear aggregation of mitochondria, whereas higher concentrations (100-250 microM) induced CoQ(10) depletion, plasma membrane perforations, mitochondrial damage, and nuclear DNA condensation and fragmentation. FeSO(4)-induced deleterious changes were attenuated by pretreatment with CoQ(10) and by deferoxamine, a potent iron chelator, in SK-N-SH cells. 1-Methyl, 4-phenyl, 1,2,3,6- tetrahydropyridine (MPTP)-induced striatal release of free iron, and NF-kappaB expression were significantly increased; whereas ferritin and melanin synthesis were significantly reduced in the substantia nigra pars compacta (SNpc) of MT(dko) mice as compared with control(wt) mice, MT(trans) mice, and alpha-synko mice. CoQ(10) treatment inhibited MPTP-induced NF-kappaB induction in all of the genotypes. These data suggest that glutathione and metallothionein synthesis might be induced as an attempt to combat iron-induced oxidative stress, whereas exogenous administration of CoQ(10) or of metallothionein induction might provide CoQ(10)-mediated neuroprotection in PD.
- Published
- 2006
13. Increased blood oxidative stress in amphetamine users
- Author
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Jatuporn Namyen, Yupin Sanvarinda, Sirinthorn Pinweha, Parichart Boontem, Patcharee Kooncumchoo, Piyarat Govitrapong, and Smith Vatanatunyakum
- Subjects
Adult ,Male ,Antioxidant ,Thiobarbituric acid ,Dopamine ,medicine.medical_treatment ,Amphetamine-Related Disorders ,Medicine (miscellaneous) ,Pharmacology ,medicine.disease_cause ,Superoxide dismutase ,Lipid peroxidation ,Young Adult ,chemistry.chemical_compound ,Reference Values ,medicine ,Humans ,Amphetamine ,chemistry.chemical_classification ,Glutathione Peroxidase ,biology ,Superoxide Dismutase ,Glutathione peroxidase ,Neurotoxicity ,Catalase ,medicine.disease ,Oxidative Stress ,Psychiatry and Mental health ,Biochemistry ,chemistry ,Chronic Disease ,biology.protein ,3,4-Dihydroxyphenylacetic Acid ,Female ,Lipid Peroxidation ,Reactive Oxygen Species ,Oxidative stress ,medicine.drug - Abstract
Amphetamine derivatives have been shown to be a potential brain neurotoxin based on the production of free radicals that occurs after administration. The purpose of this study was to examine the lipid peroxidation and antioxidant enzymes in the blood of amphetamine users. The plasma lipid peroxidation was determined and reported as thiobarbituric acid reactive substance and was significantly increased (+21%), whereas the activities of the erythrocyte antioxidant enzymes glutathione peroxidase, catalase, and superoxide dismutase were significantly decreased (-32%, -14% and -31%, respectively) in amphetamine users. These results implicated the potential role of oxidative stress in amphetamine-induced neurotoxicity.
- Published
- 2010
14. 1-Methyl-4-phenyl-pyridinium ion-induced oxidative stress, c-Jun phosphorylation and DNA fragmentation factor-45 cleavage in SK-N-SH cells are averted by selegiline
- Author
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Banthit Chetsawang, Piyarat Govitrapong, Patcharee Kooncumchoo, and Manuchair Ebadi
- Subjects
1-Methyl-4-phenylpyridinium ,Cell Survival ,Proto-Oncogene Proteins c-jun ,Substantia nigra ,Oxidative phosphorylation ,Biology ,medicine.disease_cause ,Neuroprotection ,Lipid peroxidation ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Cell Line, Tumor ,Selegiline ,medicine ,Serine ,Humans ,Phosphorylation ,Neurons ,Cell Death ,Dose-Response Relationship, Drug ,Pars compacta ,Herbicides ,JNK Mitogen-Activated Protein Kinases ,Proteins ,Parkinson Disease ,Cell Biology ,Cell biology ,Oxidative Stress ,Neuroprotective Agents ,Biochemistry ,chemistry ,DNA fragmentation ,Lipid Peroxidation ,Apoptosis Regulatory Proteins ,Reactive Oxygen Species ,Oxidative stress ,medicine.drug ,Signal Transduction - Abstract
Parkinson’s disease is a progressive neurodegenerative disorder, associated with the selective loss of dopaminergic neurons in the substantia nigra pars compacta. Recent studies have shown that c-Jun-N terminal kinase pathways might be involved in the oxidative stress-induced neuronal demise. In addition, there are several studies demonstrating that selegiline protects neural cell degeneration. In view of the above, the toxic effects of MPP+ and the protective roles of selegiline were studied in cultures of human neuroblastoma (SK-N-SH) cell lines in the present study. MPP+ significantly decreased cell viability but increased reactive oxygen species formation and lipid peroxidation, and the said effects were attenuated by selegiline. MPP+ did not change the total levels of c-Jun but enhanced phosphorylation of c-Jun at Ser73 and cleavage of DNA fragmentation factor 45, which were diminished by selegiline. MPP+-treated SK-N-SH cells exhibited an irregularly shaped nuclear chromatin or DNA fragmentation, which was abolished by selegiline. These data suggest that c-Jun-N terminal kinase pathways are involved in oxidative stress-induced dopaminergic neuronal degeneration and pretreatment with selegiline affords neuroprotection by inhibiting these cell death-signaling pathways.
- Published
- 2008
15. Coenzyme Q(10) provides neuroprotection in iron-induced apoptosis in dopaminergic neurons
- Author
-
Patcharee, Kooncumchoo, Sushil, Sharma, James, Porter, Piyarat, Govitrapong, and Manuchir, Ebadi
- Subjects
Ubiquinone ,Dopamine ,Iron ,Dopamine Agents ,Coenzymes ,Siderophores ,Apoptosis ,Mice, Transgenic ,Deferoxamine ,Cell Line ,Mice ,Animals ,Humans ,Melanins ,Mice, Knockout ,Neurons ,NF-kappa B ,Parkinson Disease ,Vitamins ,Glutathione ,Mice, Inbred C57BL ,Neuroprotective Agents ,1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ,Metallothionein ,Lipid Peroxidation ,Reactive Oxygen Species - Abstract
The exact molecular mechanism of progressive loss of neuromelanin containing nigrostriatal dopaminergic neurons in Parkinson's disease (PD) remains unknown, yet evidence suggests that iron might play an important role in PD pathology. In this study we have determined the neuroprotective role of coenzyme Q(10) (CoQ(10)) in ironinduced apoptosis in cultured human dopaminergic (SK-N-SH) neurons, in metallothionein gene- manipulated mice, and in alpha-synuclein knockout (alpha-synko) mice with a primary objective to assess a possible therapeutic and anti-inflammatory potential for CoQ(10) in PD. Iron-induced mitochondrial damage and apoptosis were characterized by reactive oxygen species production, increased metallothionein and glutathione synthesis, caspase- 3 activation, NF-kappaB induction, and decreased Bcl-2 expression, without any significant change in Bax expression. Lower concentrations of FeSO4 (1-10 microM) induced perinuclear aggregation of mitochondria, whereas higher concentrations (100-250 microM) induced CoQ(10) depletion, plasma membrane perforations, mitochondrial damage, and nuclear DNA condensation and fragmentation. FeSO(4)-induced deleterious changes were attenuated by pretreatment with CoQ(10) and by deferoxamine, a potent iron chelator, in SK-N-SH cells. 1-Methyl, 4-phenyl, 1,2,3,6- tetrahydropyridine (MPTP)-induced striatal release of free iron, and NF-kappaB expression were significantly increased; whereas ferritin and melanin synthesis were significantly reduced in the substantia nigra pars compacta (SNpc) of MT(dko) mice as compared with control(wt) mice, MT(trans) mice, and alpha-synko mice. CoQ(10) treatment inhibited MPTP-induced NF-kappaB induction in all of the genotypes. These data suggest that glutathione and metallothionein synthesis might be induced as an attempt to combat iron-induced oxidative stress, whereas exogenous administration of CoQ(10) or of metallothionein induction might provide CoQ(10)-mediated neuroprotection in PD.
- Published
- 2005
16. Salsolinol, an Endogenous Neurotoxin, Activates JNK and NF-κB Signaling Pathways in Human Neuroblastoma Cells.
- Author
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Sawitri Wanpen, Patcharee Kooncumchoo, Shaik Shavali, and Piyarat Govitrapong
- Subjects
- *
NEUROTOXIC agents , *NEUROBLASTOMA , *DOPAMINERGIC neurons , *PARKINSON'S disease - Abstract
Abstract??Salsolinol, an endogenous neurotoxin, is known to be involved in the pathogenesis of Parkinson?s disease (PD). In the present study, we have investigated the effects of salsolinol on the activation of two different signaling pathways that involve c-Jun N-terminal kinase (JNK), and nuclear factor-?B, (NF-?B) in human dopaminergic neuroblastoma SH-SY5Y cells. Salsolinol treatment caused upregulation in the levels of c-Jun and phosphorylated c-Jun. It also caused degradation of I?B? and translocated the active NF-?B into the nucleus. The binding activity of NF-?B to DNA was enhanced by salsolinol in a concentration dependent manner. Furthermore, salsolinol decreased the levels of the anti-apoptotic protein Bcl-2, and increased pro-apoptotic protein Bax, while enhancing the release of cytochrome-cfrom mitochondria. Mitochondrial complex-I activity was significantly decreased and reactive oxygen species (ROS) were increased in salsolinol treated cells. These results partly suggest that salsolinol-induced JNK and NF-?B signaling pathways may be involved in induction of apoptosis in human dopaminergic neurons, as seen in Parkinson?s disease. [ABSTRACT FROM AUTHOR]
- Published
- 2007
- Full Text
- View/download PDF
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