• Biomolecules & Therapeutics
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• 제2권1호
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• pp.1-10
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• 1994

• 대한임상약리학회:학술대회논문집
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• 대한임상약리학회 1993년도 제2차 춘계 심포지움
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• pp.7-7
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• 1993

• 한국동물학회:학술대회논문집
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• 한국동물학회 1996년도 공동 춘계학술대회
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• pp.47.2-47
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• 1996

No Abstract, See Full Text

• Journal of Korean Neurosurgical Society
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• 제67권3호
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• pp.261-264
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• 2024

• 대한영상의학회지
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• 제85권2호
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• pp.482-483
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• 2024

• 대한영상의학회지
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• 제85권2호
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• pp.480-481
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• 2024

• PNF and Movement
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• 제5권1호
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• pp.19-28
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• 2007

Proprioception means the ability to perceive the sensation of position and movement of body. As it is transmitted to central nervous system and used in feed-back or feed-forward motor control, proprioception allows us to keep our normal movement and normal balance activity. However, the conditions such as injury, disease, aging and fatigue can damage the proprioceptiive sensation of position, movement and lead to a functional impairment and additional damages in musculoskeletal system, because they alter the amount of proprioceptive ability that transfer into the central nervous system. The purpose of this study was to identify the definition and the function of proprioception, to look into variations in injury, disease, aging and fatigue that can be easily met in clinical application and eventually to provide valuable aid for assessment and treatment.

• Annals of Clinical Neurophysiology
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• 제10권2호
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• pp.98-100
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• 2008

Restless legs syndrome (RLS) is a sensorimotor neurological disorder in which the primary symptom is a compelling urge to move the legs, accompanied by unpleasant and disturbing sensations in the legs. Although pathophysiologic mechanism of RLS is still unclear, several evidences suggest that RLS is related to dysfunction in central nervous system involving brain and spinal cord. L-DOPA, as the precursor of dopamine, as well as dopamine agonists, plays an essential role in the treatment of RLS leading to the assumption of a key role of dopamine function in the pathophysiology of RLS. Patients with RLS have lower levels of dopamine in the substantia nigra and respond to iron administration. Iron, as a cofactor in dopamine production, plays a central role in the etiology of RLS. Functional neuroimaging studies using PET and SPECT support a central striatal D2 receptor abnormality in the pathophysiology of RLS. Functional MRI suggested a central generator of periodic limb movements during sleep (PLMs) in RLS. However, to date, we have no direct evidence of pathogenic mechanisms of RLS.

• BMB Reports
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• 제57권4호
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• pp.167-175
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• 2024

Cancer progression is driven by genetic mutations, environmental factors, and intricate interactions within the tumor microenvironment (TME). The TME comprises of diverse cell types, such as cancer cells, immune cells, stromal cells, and neuronal cells. These cells mutually influence each other through various factors, including cytokines, vascular perfusion, and matrix stiffness. In the initial or developmental stage of cancer, neurotrophic factors such as nerve growth factor, brain-derived neurotrophic factor, and glial cell line-derived neurotrophic factor are associated with poor prognosis of various cancers by communicating with cancer cells, immune cells, and peripheral nerves within the TME. Over the past decade, research has been conducted to prevent cancer growth by controlling the activation of neurotrophic factors within tumors, exhibiting a novel attemt in cancer treatment with promising results. More recently, research focusing on controlling cancer growth through regulation of the autonomic nervous system, including the sympathetic and parasympathetic nervous systems, has gained significant attention. Sympathetic signaling predominantly promotes tumor progression, while the role of parasympathetic signaling varies among different cancer types. Neurotransmitters released from these signalings can directly or indirectly affect tumor cells or immune cells within the TME. Additionally, sensory nerve significantly promotes cancer progression. In the advanced stage of cancer, cancer-associated cachexia occurs, characterized by tissue wasting and reduced quality of life. This process involves the pathways via brainstem growth and differentiation factor 15-glial cell line-derived neurotrophic factor receptor alpha-like signaling and hypothalamic proopiomelanocortin neurons. Our review highlights the critical role of neurotrophic factors as well as central nervous system on the progression of cancer, offering promising avenues for targeted therapeutic strategies.

• The Korean Journal of Pain
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• 제37권2호
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• pp.91-106
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• 2024

The mechanisms of the chronic pain and depression comorbidity have gained significant attention in recent years. The complement system, widely involved in central nervous system diseases and mediating non-specific immune mechanisms in the body, remains incompletely understood in its involvement in the comorbidity mechanisms of chronic pain and depression. This review aims to consolidate the findings from recent studies on the complement system in chronic pain and depression, proposing that it may serve as a promising shared therapeutic target for both conditions. Complement proteins C1q, C3, C5, as well as their cleavage products C3a and C5a, along with the associated receptors C3aR, CR3, and C5aR, are believed to have significant implications in the comorbid mechanism. The primary potential mechanisms encompass the involvement of the complement cascade C1q/C3-CR3 in the activation of microglia and synaptic pruning in the amygdala and hippocampus, the role of complement cascade C3/C3a-C3aR in the interaction between astrocytes and microglia, leading to synaptic pruning, and the C3a-C3aR axis and C5a-C5aR axis to trigger inflammation within the central nervous system. We focus on studies on the role of the complement system in the comorbid mechanisms of chronic pain and depression.