Shoulder Pain Caused by Injuries in Korean Elite Archers / 대한스포츠의학회지

Purpose@#There has been a lack of study on the pains of Korean archers, who have been getting remarkable results in international competitions. In this study, we investigated the epidemiology of shoulder pain, which is known as the most commonly complained symptom of Korean archers. @*Methods@#The participants were 58 elite archers in the city of Gwangju, South Korea. The method of the study was a retrospective cohort study by questionnaire and ultrasound and physical examination. Variables of individual characteristics, training patterns, the character of pain were analyzed in different age groups. Furthermore, groups were divided into those with shoulder pain and those without pain to analyze each group’s shoulder function. @*Results@#The most common injury was shoulder injury (65.6%), and hand injury was the second-highest prevalent injury (29.3%). These two injuries were most prevalent in all age groups. Among 58 participants, 40 showed shoulder pain, but most were mild (n=30, 51.7%) and severe pain was observed in some participants (n=2, 3.5%). Mild pain was most common in each group and it showed the highest prevalence in college students (70.0%). Pain was most observed in the drawing arm, and it was triggered most when drawing the bow. In the shoulder function test category, Constant-Murley score and American Shoulder and Elbow Surgeons score were observed the lowest in the group with shoulder pain with statistical significance. @*Conclusion@#Shoulder injury had a high prevalence in Korean archers. Correspondingly, those with shoulder pain had lower shoulder function test scores.

A Study for the Anatomic Feature of Asian Tribes: In View Point of the Golden Ratio and Beauty / 체질인류학회지

We observed and measured the structures showing the golden ratio in human body. Southeast Asian tribes, Aka and Lahu who live in Thailand, Miyanmar and China mountain areas and Koreans were examined by means of facial photography. The pictures of lateral facial view were taken by the fixed method. Then the length and width of auricles were measured by Phi-matrix software (version 1.1) on the scanned images. Helix ratio were also obtained by the same method. As a results, the ratio of the ear of Southeast Asian tribes showed the golden ratio and the racial and the individual differences were noticed a little.

Relationship between Microglial Activation and Dopaminergic Neuronal Loss in 6-OHDA-induced Parkinsonian Animal Model / 체질인류학회지

This study assessed the dynamics of morphological and immunophenotypic properties of activated microglia in a 6-hydroxydopamine (6-OHDA) induced Parkinsonian animal model. Neurodegeneration in the substantia nigra pars compacta (SNc) was induced by unilateral injection of 6-OHDA into the medial forebrain bundle. Parkinsonian animal model were sacrificed at 1, 2, 4 and 8 weeks after 6-OHDA injection. Changes in the functional activity of activated microglia were identified using different monoclonal antibodies: OX6 for major histocompatibility complex (MHC) class II, ED1 for phagocytic activity. Phagocytic microglia, characterized by ED1- or OX6-immunoreactivity, appeared in the SNc at 1 week after 6-OHDA injection, activated microglia selectively adhered to degenerating axons, dendrites and dopaminergic neuron somas in the SNc. This was followed by significant loss of these fibers and nigral dopaminergic neurons. Activation of microglia into phagocytic stage was most pronounced at 2 week after 6-OHDA injection and gradually subsided, but phagocytic microglia persisted until 8 weeks after 6-OHDA injection. Taken together, our results indicate that activated microglia is lead to persistently neuron cell death and promotes loss of dopaminergic neuron by degeneration of the dopaminergic neurons.

Selective Susceptibility of Synovial Fibroblasts Isolated from Patients with Rheumatoid Arthritis to TRAIL -induced Cell Death / 체질인류학회지

TNF -related apoptosis inducing ligand (TRAIL) is a member of TNF ligand superfamily. TRAIL transduces death signal through two distinct receptors, TRAILR -1I and TRAILR -2, while the engagement of TRAILR -3 and TRAILR -4 interferes with TRAIL -induced apoptosis. The profile of TRAILR expression has been reported to be a mechanism by which transformed cells undergo apoptosis in response to TRAIL while normal cells do not. Rheumatoid arthritis (RA) is an inflammatory autoimmune disease which is characterized by the hyperplasia of synovial membrane. The dysregulation of apoptosis in synoviocytes has been suggested to contribute to synovial hyperplasia. Synovial fibroblasts obtained from patients with RA have been reported to exhibit several semi - transformed aspects. To investigate whether RA synovial fibroblasts acquire the susceptibility to TRAIL -induced apoptosis, synovial fibroblast lines obtained from 2 RA patients and two osteoarthritis (OA) patients were cultured in the presence of recombinant human TRAIL and followed by MTT assay. TRAIL treatment resulted in a significant decrease in the viability of both lines of RA cells, indicating TRAIL -induced cell death of RA synovial fibroblasts, whereas OA synovial fibroblasts and normal human dermal fibroblasts were either resistant or less sensitive to TRAIL as compared with RA synovial fibroblasts. In RT -PCR analyses, the expression levels of TRAILR 4 in RA synovial fibroblasts were lower than in OA synovial fibroblasts, while other receptors in both cell lines were expressed at comparable levels. Immunohistochemical studies showed that in RA synovial tissues TRAILR -3cells were mainly leukocyte infiltrates, implying that such leukocyte infiltrates play a role in the perpetuation of the disease. Taken together, these results suggest that RA synovial fibroblasts acquire the susceptibility to TRAIL -induced cell death during disease progression and this death signal may be regulated by, at least in part, differential expression of TRAILR -4 molecule.

An Morphological Study on the Alteration of Immunoreactivity of the Neural Cell Adhesion molecule ( NCAM ) in Rat Spinal Cord after Unilateral Sciatic Neurotomy and Reconnection

BACKGROUND: NCAM plays an important role in the peripheral innervation of the spinal neurons as well as in the development of the CNS. Although expression of NCAM is down-regulated in most areas of adult brain and spinal cord, it could be reexpressed after neuronal damages induced by various physical or chemical insults including peripheral nerve transection. METHOD: To investigate alterations of the NCAM immunoreactivity in the dorsal and ventral horns of the spinal cord induced by peripheral neurotomy and reconnection, the unilateral sciatic nerve of the rats were transected and immediately reconnected. Experimental animals were sacrificed at 1 week and 3 weeks after operation, and the alteration of NCAM immunoreactivity in the ventral and the dorsal horns of the lower lumbar spinal cord were examined. RESULTS: NCAM-immunoreactive astrocytes in the ipsilateral dorsal horn was increased at 1 week after operation. Neurons with NCAM?immunoreactive membranes and processes were increased in ipsilateral dorsal horns, and in large motor neurons of ventral horns of both sides at 3 weeks after unilateral sciatic neurotomy and reconnection. CONCLUSIONS: It is consequently suggested that unilateral sciatic neurotomy and reconnection induce the increase of the NCAM-immunoreactive neurons and glial cells in the spinal cord, and increase of NCAM immunoreactivity in the spinal cord may reflect the neuronal damage and healing process induced by peripheral nerve injury.

Effect of (R-)-N6-phenylisopropyladenosine (RPIA) Pretreatment on the alteration of Netural Cell dhesion Molecule / 대한간질학회지

BACKGROUND: Various neuronal and glial factors which participate in neural differentiation, including neural cell adhesion molecule (NCAM), are upregulated in pathogenesis of temporal lobe epilesy (TLE).This study aimed to investigate hte effect of (R-)-N6-phenylisopropyladenosine (RPIA), an adenosine A1 receptor agonist, on the morphological alteration of NCAM immunoreactivity (IR) in limbic system of Kainic acid (KA)-induced epileptic rats. METHODS: Experiment animals were divided into control group, KA treatment only (10 mg/kg. i.p.)group, and RPIA pretreatment (100 microgram/kg. i,p, 10 min prior to injection of KA) group. Animals were sacrificed at 24 hours and 1 week after KA treatment. Luxol fast blue-cresyl violet stain for histopathological observation, and NCAM immunohistochemistry to study alteration of NCAM IR in limbic system were performed. RESULTS: Neuronal loss in CA1 and CA3areas of hippocampus, piridorm cortex, basolateral amygdala nucleus and lateral dorsal thalamic nucleus were induced by KA unjection, and thoes were reduced by RPIA pretreatment. Inrease of NCAM-IR was observed in interneurons of all hippocampal areas. except CA2 area, pirform cortex and basolateral amygdala nucleus at 24 hours after KA injection. and increased NCAM-IR was observed in cell membrane and processes of neuroglia, dentate granule cells and pyramidal cells in CA1 area of hippocampus. and neurons in piriform cortex, amygdala and lateral dorsal thalamic nucleus 1 week after KA injection, but those changes were milder than those at 24 hours after KA injection. RPIA pretreatment significantly reduced KA-induced NCAM-IR in hippocampal CA3, CA1 area, piriform cortex, amtgdala and lateral dorsal thalamic nucleus. CONCLUSION: We suggest that decrease of NCAM immunoreactivity is associated with neuprotective effects of RPIA on limbic system against KA neurotoxiciy.

Effects of Ischemic Preconditioning, Adenosine and Pinacidil on Expression of Apoptosis in the Rectus Femoris Muscles of the Rats after Ischemia and Timely Reperfusion / 체질인류학회지

The ischemia and reperfusion injury of skeletal muscle is caused by generation of reactive oxygen species. Recently, apoptosis has been associated with oxidative stress in a number of cell systems. The effects of ischemic preconditoining in cardiac muscle have been established as rendering muscle tolerance to ischemic reperfusion damage via opening of KAPT channel and activation of adenosine A1 receptor. The effects and mechanisms of ischemic preconditioning are not known clearly. The present study was performed to investigate the effect and the mechanisms of ischemic preconditioning by measuring the incidences of apoptosis on timely reperfused ischemic muscles. The healthy Sprague -Dawley rats weighing from 200 g to 250 g were used as experimental animals. Under pentobarbital (50 mg/kg) anesthesia, lower abdominal incision was done and left common iliac artery was ligated by using vascular clamp for 2 hours. Rectus femoris muscles were obtained at 0 hour, 1 hour, 2 hours, 6 hours, 12 hours and 24 hours of reperfusion. The group of ischemic preconditioning underwent three episodes of 5 minutes occlusion and 5 minutes reperfusion of common iliac artery followed by 2 hours of ischemia and timely reperfusion. Adenosine (50 microgram/kg) or pinacidil (1 mg/kg) were administered intravenously before ischemia and 2 hours of ischemia and timely reperfusion was done. 6 microM of paraffin sections were obtained. The incidencies of apoptosis were observed by use of in situ apoptosis detection kit. The results obtained were as follows. 1. The reactivities to apoptosis in the rectus femoris muscle increased after 2 hours of ischemia and timely reperfusion. 2. After 2 hours of ischemia and timely reperfusion with ischemic preconditioning and the treatment of pinacidil, the reactivities to apoptosis in all groups decreased markedly. 3. After 2 hours of ischemia and timely reperfusion with the treatment of adenosine, the reactivities to apoptosis in all groups were similar to those in the group of 2 hours of ischemia and reperfusion. Consequently, these results suggest that the reactivities to apoptosis decrease after 2 hours of ischemia and timely reperfusion with ischemic preconditioning. The effect of ischemic preconditioning is related to opening of KATP channel partly.