Cardiorespiratory Performance, Physical Activity, and Depression in Thai Older Adults with Sarcopenia and No Sarcopenia: A Matched Case-Control Study.

BACKGROUND: Older adults have a high risk for musculoskeletal, cardiorespiratory, and mental health problems. We compared respiratory muscle strength, cardiovascular endurance, physical activity (PA), and depression between older adults with and without sarcopenia. METHODS: This matched case-control study included 200 Thai older adults (100 participants with and without sarcopenia). According to the Asian Working Group for Sarcopenia 2019, participants completed a handgrip dynamometer, a 6 m walk test, and bioimpedance analysis for sarcopenia screening. Individuals were required to evaluate their cardiovascular endurance and respiratory muscle strength and complete a set of questionnaires (i.e., depression and PA). Participants with and without sarcopenia were compared using a t-test, and ANOVA was used for subgroup analysis. RESULTS: Participants with sarcopenia had significantly lower inspiratory muscle strength (p < 0.001), functional capacity (p = 0.032), PA (p < 0.001), and higher depression scores (p < 0.001) than those without sarcopenia. Respiratory muscle strength and PA were significantly reduced in those with severe sarcopenia, followed by those with sarcopenia, possible sarcopenia, and no sarcopenia. Older adults with severe sarcopenia had higher depression scores than those with sarcopenia, possible sarcopenia, or no sarcopenia. CONCLUSIONS: Older adults with sarcopenia may exhibit lower cardiorespiratory performance, less PA, and higher depression than those without sarcopenia.

Gait Improvement in Chronic Stroke Survivors by Using an Innovative Gait Training Machine: A Randomized Controlled Trial.

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.

Acute effects of air pollution on all-cause mortality: a natural experiment from haze control measures in Chiang Mai Province, Thailand.

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 <10 micron in aerodynamic diameter (PM10), gaseous pollutants (SO2, NO2, O3, and CO), and meteorology in Chiang Mai Province between January 2002 and December 2016. We analyzed the data using a case-crossover approach adjusting for temperature, relative humidity, seasonality, and day-of-week. We assessed change in the excess risks of all-cause mortality associated with an increase in interquartile range (IQR) of pollutant concentration before and after control measures came into force. RESULTS: We found decreased PM10 levels and markedly reduced excess risks of daily mortality associated with an IQR increase in PM10 concentrations in the years after haze-control measures were implemented (2009-2016). We found mixed results for gaseous pollutants: SO2 showed no significant change in excess risk of daily mortality throughout the study period, while NO2 and CO showed significant excess risks only in the period 2012-2016, and 8-h maximum O3 showed a decrease in excess risk despite an increase in its atmospheric levels after the introduction of haze control measures in 2008. CONCLUSIONS: The findings indicate that the government haze control measures first introduced in Chiang Mai province in 2008 have successfully reduced episodic PM10 concentrations, which has led to a decrease in short-term all-cause mortality.

Increased blood oxidative stress in amphetamine users.

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.

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.

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.

Salsolinol, an endogenous neurotoxin, activates JNK and NF-kappaB signaling pathways in human neuroblastoma cells.

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.

Coenzyme Q(10) provides neuroprotection in iron-induced apoptosis in dopaminergic neurons.

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.