• 대한인간공학회지
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• 제34권5호
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• pp.363-375
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• 2015

Objective: This study aims to recognize the risk of current traffic systems and to investigate a method to decrease risk by doing exercise using an elastic-band and cognitive rehabilitation. Background: The existing traffic system usually focuses on the ordinary citizens, which may not be appropriate to the elderly. It may affect the cognition and walking speed of the elderly. This study tries to examine whether cognition and muscle training is appropriate to improve their vulnerability. Therefore this study will provide human ergonomics - based basic data in relation to the elderly to identify the risk of current signal system and to mitigate the risk. Method: A total of 30 elderly participants were divided into two groups: experimental and control groups. Experimental group (n=15) was trained to strengthen their muscles and to promote cognition, whereas control group (n=15) was not. The training was conducted twice a week for three weeks. To strengthen muscles, a yellow colored elastic-band was used, and a computer program for cognitive rehabilitation was used to develop cognition. In the experimental group, there were significant differences between pre and post exercises However, the control group didn't show any significant difference. The increase in cognition and walking speed was found in the experimental group, whereas there were no differences in the control group. Statistically there was no significant difference between the two groups. Results: The results of this study show that the exercise program using the elastic-band gave a positive effect on gait training thanks to the development of muscle power and balance. Conclusion: This study did not show any statistical difference or significant differences between the two groups, since time was restricted, we believe. Application: The results of the walking speed will help to prevent traffic collision.

• Biomolecules & Therapeutics
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• 제31권2호
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• pp.161-167
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• 2023

Despite the various medications used in clinics, the efforts to develop more effective treatments for depression continue to increase in the past decades mainly because of the treatment-resistant population, and the testing of several hypotheses- and target-based treatments. Undesirable side effects and unresponsiveness to current medications fuel the drive to solve this top global health problem. In this study, we focused on neuroinflammatory response-mediated depression which represents a cluster of depression etiology both in animal models and humans. Several meta-analyses reported that proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were increased in major depressive disorder patients. Inflammatory mediators implicated in depression include type-I interferon and inflammasome pathways. To elucidate the molecular mechanisms of neuroinflammatory cascades underlying the pathophysiology of depression, we introduced hycanthone, an antischistosomal drug, to check whether it can counteract depressive-like behaviors in vivo and normalize the inflammation-induced changes in vitro. Lipopolysaccharide (LPS) treatment increased proinflammatory cytokine expression in the murine microglial cells as well as the stimulation of type I interferon-related pathways that are directly or indirectly regulated by Janus kinase-signal transducer and activator of transcription (JAK-STAT) activation. Hycanthone treatment attenuated those changes possibly by inhibiting the JAK-STAT pathway and inflammasome activation. Hycanthone also ameliorated depressive-like behaviors by LPS. Taken together, we suggest that the inhibitory action of hycanthone against the interferon pathway leading to attenuation of depressive-like behaviors can be a novel therapeutic mechanism for treating depression.