Sookyoung Park

Melatonin plus exercise-based neurorehabilitative therapy for spinal cord injury.

Abstract:u2002 Spinal cord injury (SCI) is damage to the spinal cord caused by the trauma or disease that results in compromised or loss of body function. Subsequent to SCI in humans, many individuals have residual motor and sensory deficits that impair functional performance and quality of life. The available treatments for SCI are rehabilitation therapy, activity‐based therapies, and pharmacological treatment using antioxidants and their agonists. Among pharmacological treatments, the most efficient and commonly used antioxidant for experimental SCI treatment is melatonin, an indolamine secreted by pineal gland at night. Melatonin’s receptor‐independent free radical scavenging action and its broad‐spectrum antioxidant activity makes it an ideal antioxidant to protect tissue from oxidative stress‐induced secondary damage after SCI. Owing to the limitations of an activity‐based therapy and antioxidant treatment singly on the functional recovery and oxidative stress‐induced secondary damages after SCI, a melatonin plus exercise treatment may be a more effective therapy for SCI. As suggested herein, supplementation with melatonin in conjunction with exercise not only would improve the functional recovery by enhancing the beneficial effects of exercise but would reduce the secondary tissue damage simultaneously. Finally, melatonin may protect against exercise‐induced fatigue and impairments. In this review, based on the documented evidence regarding the beneficial effects of melatonin, activity‐based therapy and the combination of both on functional recovery, as well as reduction of secondary damage caused by oxidative stress after SCI, we suggest the melatonin combined with exercise would be a novel neurorehabilitative strategy for the faster recovery after SCI.

Synergistic effect of melatonin on exercise‐induced neuronal reconstruction and functional recovery in a spinal cord injury animal model

Abstract:u2002 Nitric oxide (NO) may aggravate neuronal damage after spinal cord injury (SCI). We hypothesized that NO produced by inducible nitric oxide synthase (iNOS) accelerates secondary damage to spinal tissue, which may be reversed by the neuroprotectant, melatonin. This study investigated the effects of combination therapy with melatonin (10u2003mg/kg) and exercise (10u2003m/min) on recovery from SCI caused by contusion. We examined locomotor recovery, iNOS gene expression, autophagic and apoptotic signaling, including Beclin‐1, LC3, p53 and IKKα protein expression and histological alterations in the ventral horn of the spinal cord. Melatonin in combination with exercise resulted in significantly increased hindlimb movement (Pu2003<u20030.05), a reduced level of iNOS mRNA (Pu2003<u20030.05) and more motor neurons in the ventral horn, versus control SCI and SCI plus exercise alone, with no effect on the other signaling molecules examined. This study shows that combined therapy with melatonin and exercise reduces the degree of secondary damage associated with SCI in rats and supports the possible use of melatonin in combination with exercise to reduce the side effects related to exercise‐induced fatigue and impairment.

Beneficial effects of endogenous and exogenous melatonin on neural reconstruction and functional recovery in an animal model of spinal cord injury.

Abstract:u2002 The purpose of this study was to investigate the beneficial effects of endogenous and exogenous melatonin on functional recovery in an animal model of spinal cord injury (SCI). Eight‐week‐old male Sprague‐Dawley (SD, 250–260u2003g) rats were used for contusion SCI surgery. All experimental groups were maintained under one of the following conditions: 12/12‐hr light/dark (L/D) or 24:0‐hr constant light (LL). Melatonin (10u2003mg/kg) was injected subcutaneously for 4u2003wk, twice daily (07:00, 19:00). Locomotor recovery, inducible nitric oxide synthase (iNOS), glial fibrillary acidic protein gene expression, and muscle atrophy‐related genes, including muscle atrophy F‐box (MAFbx) and muscle‐specific ring‐finger protein 1 (MuRF1) gene expression were evaluated. Furthermore, autophagic signaling such as Beclin‐1 and LC3 protein expression was examined in the spinal cord and in skeletal muscle. The melatonin treatment resulted in increased hind‐limb motor function and decreased iNOS mRNA expression in the L/D condition compared with the LL condition (Pu2003<u20030.05), indicating that endogenous melatonin had neuroprotective effects. Furthermore, the MAFbx, MuRF1 mRNA level, and converted LC3 II protein expression were decreased in the melatonin‐treated SCI groups under the LL (Pu2003<u20030.05), possibly in response to the exogenous melatonin treatment. Therefore, it seems that both endogenous and exogenous melatonin contribute to neural recovery and to the prevention of skeletal muscle atrophy, promoting functional recovery after SCI. Finally, this study supports the benefit of endogenous melatonin and use of exogenous melatonin as a therapeutic intervention for SCI.

The effects of smartphone use on upper extremity muscle activity and pain threshold

[Purpose] The purpose of this study was to determine whether muscle activity and pressure-induced pain in the upper extremities are affected by smartphone use, and to compare the effects of phone handling with one hand and with both hands. [Subjects] The study subjects were asymptomatic women 20–22u2005years of age. [Methods] The subjects sat in a chair with their feet on the floor and the elbow flexed, holding a smartphone positioned on the thigh. Subsequently, the subjects typed the Korean anthem for 3u2005min, one-handed or with both hands. Each subject repeated the task three times, with a 5-min rest period between tasks to minimize fatigue. Electromyography (EMG) was used to record the muscle activity of the upper trapezius (UT), extensor pollicis longus (EPL), and abductor pollicis (AP) during phone operation. We also used a dolorimeter to measure the pressure-induced pain threshold in the UT. [Results] We observed higher muscle activity in the UT, AP, and EPL in one-handed smartphone use than in its two-handed use. The pressure-induced pain threshold of the UT was lower after use of the smartphone, especially after one-handed use. [Conclusion] Our results show that smartphone operation with one hand caused greater UT pain and induced increased upper extremity muscle activity.

Comparison of surgical methods of transient middle cerebral artery occlusion between rats and mice.

Rodent models of focal cerebral ischemia that do not require craniotomy have been developed by intraluminal suture middle cerebral artery occlusion (MCAo). Mouse MCAo models have been widely used and extended to genetic studies of cell death or recovery mechanisms. Therefore, we compared surgery-related parameters and techniques between such rats and mice. In rodent MCAo models, has to be considered body temperature during the operative period, as well as the need for the use of a standardized tip in terms of the outer diameter of probes. Induction of focal cerebral ischemia was measured by neurological dysfunction parameters. Our methods could induce stable moderate-severity ischemic brain injury models and histological alteration at 24 hr after MCAo surgery. Moreover approximately 80% (rats) and 85% (mice) survival ratios were shown indicating with model engineering success. Finally, we described and compared major parameters between rats and mice, including probe size, thread insert length, operation and occlusion periods, and differences in the procedures.

Therapeutic physical exercise in neural injury: friend or foe?

[Purpose] The intensity of therapeutic physical exercise is complex and sometimes controversial in patients with neural injuries. This review assessed whether therapeutic physical exercise is beneficial according to the intensity of the physical exercise. [Methods] The authors identified clinically or scientifically relevant articles from PubMed that met the inclusion criteria. [Results] Exercise training can improve body strength and lead to the physiological adaptation of skeletal muscles and the nervous system after neural injuries. Furthermore, neurophysiological and neuropathological studies show differences in the beneficial effects of forced therapeutic exercise in patients with severe or mild neural injuries. Forced exercise alters the distribution of muscle fiber types in patients with neural injuries. Based on several animal studies, forced exercise may promote functional recovery following cerebral ischemia via signaling molecules in ischemic brain regions. [Conclusions] This review describes several types of therapeutic forced exercise and the controversy regarding the therapeutic effects in experimental animals versus humans with neural injuries. This review also provides a therapeutic strategy for physical therapists that grades the intensity of forced exercise according to the level of neural injury.

Differential expression of caveolins and myosin heavy chains in response to forced exercise in rats

Exercise training can improve strength and lead to adaptations in the skeletal muscle and nervous systems. Skeletal muscles can develop into two types: fast and slow, depending on the expression pattern of myosin heavy chain (MHC) isoforms. Previous studies reported that exercise altered the distribution of muscle fiber types. It is not currently known what changes in the expression of caveolins and types of muscle fiber occur in response to the intensity of exercise. This study determined the changes in expression of caveolins and MHC type after forced exercise in muscular and non-muscular tissues in rats. A control (Con) group to which forced exercise was not applied and an exercise (Ex) group to which forced exercise was applied. Forced exercise, using a treadmill, was introduced at a speed of 25 m/min for 30 min, 3 times/day (07:00, 15:00, 23:00). Homogenized tissues were applied to extract of total RNA for further gene analysis. The expression of caveolin-3 and MHC2a in the gastrocnemius muscle of female rats significantly increased in the Ex group compared with the Con group (P<0.05). Furthermore, in the gastrocnemius muscle of male rats, the expression of MHC2x was significantly different between the two groups (P<0.05). There was an increased expression in caveolin-3 and a slightly decreased expression in TGFβ-1 in muscular tissues implicating caveolin-3 influences the expression of MHC isoforms and TGFβ-1 expression. Eventually, it implicates that caveolin-3 has positive regulatory function in muscle atrophy induced by neural dysfunction with spinal cord injury or stroke.