Earticle

체육학에서 운동역학 및 초등체육 관련 운동역학 연구의 현실과 문제점을 알아보고 활성화 시킬 수 있는 방안에대해서 알아보고자 하였다. 한국체육학회지, 한국운동역학회지, 그리고 한국초등체육학회지에 게재된 논문을 대상으로 분석한 결과는 다음과 같다. 최근 3년(2012～2014)간 운동역학 관련 연구를 분석한 결과, 연구 내용에 따라서 운동기술분석 44.5%, 측정 및 자료처리 38.4%, 상해관련 12.3%, 기타 10%로 나타났다. 연구 방법에 따라서는영상분석 60.7%, 근전도 10.9%, 압력판 9%로 나타났으며, 영상분석과 압력판을 이용한 연구(6.2%)와 영상분석과근전도를 이용한 분석(2%), 그리고 기타의 방법(15.2%) 등을 이용한 것으로 나타났다. 최근 5년(2009～2014)간 초등체육과 관련한 운동역학 연구는 한국체육학회지 0.1%, 한국운동역학회지 1.3%, 한국초등체육학회지 4.5%로 나타났다. 연구내용은 운동기술분석(66.7%), 측정 및 자료처리와 상해관련(각각 16.7%)의 연구였으며, 연구방법으로는 영상분석 관련 연구가 대부분(83.3%)을 차지하였다. 이처럼 운동역학 관련, 특히 초등체육에서의 연구가 미진한 이유는 연구여건의 미비, 전문 연구인력의 부족, 기초자료 부족, 그리고 연구대상자 확보와 통제의 어려움이주요 원인으로 판단된다. 따라서 전문연구 인력 및 실험실과 연구기자재의 확보, 흥미를 유발할 수 있는 편안한강의, 현장성 있는 연구와 함께 체계적인 분석 및 지도방법의 모색 등을 통해서 활성화 할 수 있도록 노력해야할 것이다.

The purpose of this study was to identify current trend and issues and to activating sport biomechanics research related to general sport science and elementary physical education. In order to achieve purpose of the study, research published in The Korean Journal of Physical Education(KJPE), Korean Journal of Sport Biomechanics(KJSB), and The Korean Journal of Elementary Physical Education(KJEPE) were analysed. Based on analysis of biomechanics research in past 3 years, motor skill analysis(44.5%) was the most frequently appeared in the studies followed by measurement and data processing(38.4%), injury(12.3%), and others(10%) respectively in terms of content of the research. Research methods used in the studies were image analysis(60.7%), electromyogram(10.9%), and pressure plate(9%). There were also studies used both image analysis and pressure plate(6.2%), image analysis and electromyogram(2%) and others(15.2%). Based on analysis of biomechanics research in past 5 years related to elementary physical education, it was shown in KJPE(0.1%), KJSB(6.2%), and KJEPE(4.5%). Research contents were motor skill analysis(66.7%), measurement and data processing, and injury(16.7%) respectively and most of research(83.3%) were used image analysis as research method. Reasons of the lack of research related to biomechanics, especially elementary physical education would be insufficiency of the research conditions, lack of professional researchers, lack of basic data, and difficulty of having and controling samples. Therefore, it should be make efforts to secure professional researchers, lab, and equipments, to make effective teaching created more interests about biomechanics, and to conduct research having more practically oriented along with systematic analysis and teaching method.

Purpose: The ascending reticular activating system (ARAS) is responsible for regulation of consciousness. In this study, using diffusion tensor imaging (DTI), we attempted to reconstruct the thalamocortical projections between the intralaminar thalamic nuclei and the frontoparietal cortex in normal subjects. Methods: DTI data were acquired in 24 healthy subjects and eight kinds of thalamocortical projections were reconstructed: the seed region of interest (ROI) - the intralaminar thalamic nuclei and the eight target ROIs - the medial prefrontal cortex, dorsolateral prefrontal cortex, ventrolateral prefrontal cortex, orbitofrontal cortex, premotor cortex, primary motor cortex, primary somatosensory cortex, and posterior parietal cortex. Results: The eight thalamocortical projections were reconstructed in each hemisphere and the pathways were visualized: projections to the prefrontal cortex ascended through the anterior limb and genu of the internal capsule and anterior corona radiata. Projections to the premotor cortex passed through the genu and posterior limb of the internal capsule and middle corona radiata; in contrast, projections to the primary motor cortex, primary somatosensory cortex, and posterior parietal cortex ascended through the posterior limb of the internal capsule. No significant difference in fractional anisotropy, mean diffusivity, and fiber volume of all reconstructed thalamocortical projections was observed between the right and left hemispheres (p>0.05). Conclusion: We reconstructed the thalamocortical projections between the intralaminar thalamic nuclei and the frontoparietal cortex in normal subjects. We believe that our findings would be useful to clinicians involved in the care of patients with impaired consciousness and for researchers in studies of the ARAS.

Water-soluble polysaccharides isolated from the rhizome of Polygonatum sibiricum and fractionated using ionexchange chromatography were investigated to determine their structure and immunostimulating activity. Crude and fractions ($F_1$ and $F_2$) consisted of carbohydrates (85.1~88.3%) with proteins (4.51~11.9%) and uronic acid (1.79~7.47%), and included different levels of mannose (62.3~76.3%), glucose (15.2~20.3%), galactose (4.35~15.3%), and arabinose (4.00~7.65%). The crude contained two peaks with molecular weights (Mw) of $151{\times}10^3$ and $31.8{\times}10^3$, but $F_1$ and $F_2$ exhibited one major peak with Mw of $103{\times}10^3$ and $628{\times}10^3$, respectively. Little immunostimulatory activity was observed by the crude; however, $F_1$ and $F_2$ significantly activated RAW264.7 cells to release nitric oxide and various cytokines, suggesting they were potent immunostimulators. The backbone of the most immunostimulating fraction ($F_1$) was ($1{\rightarrow}4$)-manno- and ($1{\rightarrow}4$)-gluco-pyranosyl residues with galactose and glucose attached to O-6 of manno-pyranoside.

Kahweol as a coffee-specific diterpene has been reported to induce apoptosis in human cancer cells. Although some molecular targets for kahweol-mediated apoptosis have been elucidated, the further mechanism for apoptotic effect of kahweol is not known. Activating transcription factor 3 (ATF3) has been reported to be associated with apoptosis in colorectal cancer. The present study was performed to investigate the molecular mechanism by which kahweol stimulates ATF3 expression and apoptosis in human colorectal cancer cells. Kahweol increased apoptosis in human colorectal cancer cells. It also increased ATF3 expression through the transcriptional activity. The responsible cis-element for ATF3 transcriptional activation by kahweol was CREB located between -147 to -85 of ATF3 promoter. ATF3 overexpression increased kahweol-mediated cleaved PARP, while ATF3 knockdown attenuated the cleavage of PARP by kahweol. Inhibition of ERK1/2 and $GSK3{\beta}$ blocked kahweol-mediated ATF3 expression. The results suggest that kahweol induces apoptosis through ATF3-mediated pathway in human colorectal cancer cells.

Objective: Low intensity pulsed ultrasound (LIPUS) has been shown to accelerate cell proliferation and tissue healing in both animal models and clinical trials. However, details of the clinical effects of LIPUS have not been well characterized. The aim of this study was to investigate the effect of LIPUS on mitogen-activated protein kinase (MAPK) activation in rat articular chondrocytes. Design: Cross-sectional study. Methods: Chondrocyte were cultured in six well cell culture plates for 72 hours at $37^{\circ}C$ with 5% $CO_2$, and then exposed to LIPUS at 1.5 MHz frequency and $30-mW/cm^2$ power. Changes in chondrocyte activities were evaluated in response to oxydative stress in dose-dependent (0 and 300 uM) and time-dependent (0-24 hr) manner. The cell viability were analyzed using MTT [3-(4.5-dimethylthiazol-2-yl)-2.5 diphenyltetrazolium bromide]. The expression of p38 MAPK was measured using western blotting. Results: Oxidative stress was induced in rat chondrocytes using hydrogen peroxide ($H_2O_2$). The cell viability was decreased in chondrocytes after the $H_2O_2$ dose and time-dependent treatment. The p38 MAPK phosphorylation occurred at a significantly increased rate after $H_2O_2$ treated (p<0.05). Expression of p38 MAPK was decreased in the p38 inhibitor groups compared with the oxidative stress-induced chondrocyte damage via the p38 MAPK signaling pathways (p<0.05). Conclusions: It could be concluded that LIPUS can inhibit oxidative stress-induced chondrocyte damage via the p38 MAPK signaling pathways.

Post-translational modifications (PTMs) play a crucial role in the regulation of protein function. Protein O-linked N-acetylglucosamine (O-GlcNAc) is a type of nutrient-sensitive PTM that occurs on serine or threonine residues of substrates, catalysed by single pair of enzymes, O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). In the present study, we have observed that serum deprivation decreased OGT levels without affecting its transcription. Instead, we found that serum deprivation activated AMP-activated protein kinase (AMPK) and induced the phosphorylation of OGT at threonine 444, resulting in the proteolysis of OGT by the CUL1/SKP1/SKP2 E3 ubiquitin ligase. Knocking down OGT significantly impaired 3T3-L1 cell differentiation in the presence of serum. Likewise, treatment with AICAR, an AMPK activator, or OSMI-1, an OGT small molecule inhibitor, attenuated serum-induced 3T3-L1 differentiation. Together, our results demonstrate that OGT is essential for 3T3 cell differentiation in which serum starvation activates AMPK to phosphorylate OGT at Thr444, triggering the proteolysis of OGT by the CUL1/SKP1/SKP2 E3 ligase.

Norovirus (NV) is the most common cause of viral gastroenteritis, with the potential to develop into a fatal disease in those who are immuno-compromised, and effective vaccines and treatments are still non-existent. In this study, we aimed to elucidate the molecular mechanism of the previously identified NV replication inhibitor utilizing a vinyl-stilbene backbone, AC-1858. First, we confirmed the inhibition of the NV RNA replication by a structural analog of AC-1858, AC-2288 with its exclusive cytoplasmic sub-cellular localization. We further validated the induction of one specific host factor, the phosphorylated form of heat shock factor (HSF)-1, and its increased nuclear localization by AC-1858 treatment. Finally, we verified the positive and negative impact of the siRNA-mediated downregulation and lentivirus-mediated overexpression of HSF-1 on NV RNA replication. In conclusion, these data suggest the restrictive role of the host factor HSF-1 in overall viral RNA genome replication during the NV life cycle.

Alopecia is a distressing condition caused by the dysregulation of anagen, catagen, and telogen in the hair cycle. Dermal papilla cells (DPCs) regulate the hair cycle and play important roles in hair growth and regeneration. Myristoleic acid (MA) increases Wnt reporter activity in DPCs. However, the action mechanisms of MA on the stimulation of anagen signaling in DPCs is not known. In this study, we evaluated the effects of MA on anagen-activating signaling pathways in DPCs. MA significantly increased DPC proliferation and stimulated the G2/M phase, accompanied by increasing cyclin A, Cdc2, and cyclin B1. To elucidate the mechanism by which MA promotes DPC proliferation, we evaluated the effect of MA on autophagy and intracellular pathways. MA induced autophagosome formation by decreasing the levels of the phospho-mammalian target of rapamycin (phospho-mTOR) and increasing autophagy-related 7 (Atg7) and microtubule-associated protein 1A/1B-light chain 3II (LC3II). MA also increased the phosphorylation levels of Wnt/β-catenin proteins, such as GSK3β (Ser9) and β-catenin (Ser552 and Ser675). Treatment with XAV939, an inhibitor of the Wnt/β-catenin pathway, attenuated the MA-induced increase in β-catenin nuclear translocation. Moreover, XAV939 reduced MA-induced effects on cell cycle progression, autophagy, and DPC proliferation. On the other hand, MA increased the levels of phospho (Thr202/Tyr204)-extracellular signal regulated kinases (ERK). MA-induced ERK phosphorylation led to changes in the expression levels of Cdc2, Atg7 and LC3II, as well as DPC proliferation. Our results suggest that MA promotes anagen signaling via autophagy and cell cycle progression by activating the Wnt/β-catenin and ERK pathways in DPCs.

Fibroblast-like synoviocytes (FLS) play a crucial role in initiating rheumatoid arthritis. B-cell activating factor (BAFF) plays a role in FLS survival as well as in B cell maturation and maintenance. Here, we investigated whether tumor necrosis factor (TNF)-α-induced BAFF expression controls FLS migration and whether BAFF expression in FLS could be regulated by KR33426 which is the inhibitor of BAFF binding to BAFF receptors (BAFF-R) by using MH7A synovial cells transfected with the SV40 T antigen. More TNF-α-treated cells migrated compared to the control. TNF-α increased BAFF expression in FLS, significantly. FLS migration was inhibited by the transfection with BAFF-siRNA. KR33426 also inhibited BAFF expression increased by TNF-α treatment in FLS as judged by western blotting, PCR, and transcriptional activity assay. Kinases including JNK, p38 and Erk were activated by TNF-α treatment. While JNK and p38 were inhibited by KR33426 treatment, no changes in Erk were observed. Transcription factors including p65, c-Fos, CREB and SP1 were enhanced by TNF-α treatment. Among them, c-Fos was inhibited by KR33426 treatment. Small interference(si)-RNA of c-fos decreased BAFF transcriptional activity. FLS migration induced by TNF-α was inhibited by the transfection with BAFF-siRNA. KR33426 increased Twist, Snail, Cadherin-11 and N-Cadherin. In contrast, KR33426 decreased E-cadherin and TNF-α-enhanced CCL2. Taken together, our results demonstrate that synovial cell migration via CCL2 expression could be regulated by BAFF expression which is decreased by KR33426 and c-Fos-siRNA. It suggests for the first time that the role of BAFF-siRNA on FLS migration might be matched in the effect of KR33426 on BAFF expression.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common clinical syndrome of diffuse lung inflammation with high mortality rates and limited therapeutic methods. Diosmetin, an active component from Chinese herbs, has long been noticed because of its antioxidant and anti-inflammatory activities. The aim of this study was to evaluate the effects of diosmetin on LPS-induced ALI model and unveil the possible mechanisms. Our results revealed that pretreatment with diosmetin effectively alleviated lung histopathological changes, which were further evaluated by lung injury scores. Diosmetin also decreased lung wet/dry ratios, as well as total protein levels, inflammatory cell infiltration and proinflammatory cytokine (eg. $TNF-{\alpha}$, $IL-1{\beta}$ and IL-6) overproduction in bronchoalveolar lavage fluid (BALF). Additionally, increased MPO, MDA and ROS levels induced by LPS were also markly suppressed by diosmetin. Furthermore, diosmetin significantly increased the expression of Nrf2 along with its target gene HO-1 and blocked the activation of NLRP3 inflammasome in the lung tissues, which might be central to the protective effects of diosmetin. Further supporting these results, in vitro experiments also showed that diosmetin activated Nrf2 and HO-1, as well as inhibited the NLRP3 inflammasome in both RAW264.7 and A549 cells. The present study highlights the protective effects of diosmetin on LPS-induced ALI via activation of Nrf2 and inhibition of NLRP3 inflammasome, bringing up the hope of its application as a therapeutic drug towards LPS-induced ALI.

Reactive oxygen species play a role in signal transduction and in many human diseases. B-cell activating factor (BAFF) plays a role for mature B cell generation and maintenance and for the incidence of autoimmune diseases. We previously reported that BAFF expression was induced by ROS. In this study, we investigated whether ROS-induced BAFF expression was affected by toll-like receptor (TLR) 4 or myeloid differentiation primary response gene (MyD) 88. BAFF expression was increased by serum deprivation that is an experimental modification to produce ROS. In contrast, TLR4 and MyD88 were decreased by serum deprivation. Although ROS production was decreased in TLR4-nonfunctional or MyD88-deficient splenocytes as compared to that in control mice, serum deprivation increased ROS production and augmented BAFF expression in both cells. $50{\mu}M\;H_2O_2$ also increased BAFF expression in TLR4-deficient or MyD88-deficient splenocytes. Collectively, results show that BAFF expression may be mediated by TLR4 or MyD88-independent manner and TLR4 or MyD88 may not be required in BAFF expression.

Since platelet-activating factor (PAF) is involved in inflammation, allergic response and anaphylactic shock, PAF receptor antagonists may have potential for controlling these disease conditions. The extract of the leaves of Ginkgo biloba having a higher content of terpenoids (12%) with flavonoids (24%) (YY1224) was prepared in order to obtain the increasing PAF antagonistic activity. As expected, YY1224 showed a higher PAF antagonistic binding affinity ($IC_{50}\;=\;0.09\;{\mu}g/ml$) using $[^3H]PAF$ and rabbit platelets as ligand and receptor source, compared with an $IC_{50}$ of $>\;100\;{\mu}g/ml$ by Egb 761, a standardized extract. YY1224 also showed a higher inhibitory activity against PAF-induced platelet aggregation and NO production from lipopolysaccharide-treated RAW 264.7 cells. In addition, it protected PAF-induced death in mice by oral administration at 15 mg/kg. All these results suggest that YY1224 may show favorable effects on PAF-related disorders.

Translationally controlled tumor protein (TCTP) is a regulatory protein that plays pivotal roles in cellular processes including the cell cycle, apoptosis, microtubule stabilization, embryo development, stress responses, and cancer. However, the molecular mechanism by which it promotes tumor angiogenesis is still unclear. In this study, we explored the mechanisms underlying stimulation of angiogenesis by a novel TCTP. Recombinant TCTP enhanced vascular endothelial growth factor (VEGF)-induced endothelial cell migration, capillary-like tubular structure formation, and cell proliferation by interacting with VEGF receptor 2 (VEGFR-2) in vitro. In contrast, we showed that TCTP knockdown (using short interfering [si]TCTP) led to a decrease in ovarian tumor cells. We also examined the expression of VEGF and hypoxia inducible factor 1 (HIF-1α), an important angiogenic factor. The expression of VEGF as well as HIF-1α was dramatically decreased by siTCTP. Mechanistically, siTCTP inhibited VEGFR-2 tyrosine phosphorylation and phosphorylation of its downstream targets PI3K, Akt, and mTOR. Collectively, these findings indicate that TCTP can promote proliferation and angiogenesis via the VEGFR-2/PI3K and mTOR signaling pathways in ovarian tumor cells, providing new insight into the mechanism behind the involvement of TCTP in tumor angiogenesis.

Albiflorin, a key active compound in the roots of Paeonia lactiflora Pall, is known to have multiple health benefits. Although albiflorin has been shown to exert its major pharmacological effects via its antioxidant activity, its efficacy in the muscles has not been evaluated. In this study, we examined the protective activity of albiflorin against oxidative injury in C2C12 murine myoblasts. C2C12 cells were pretreated with nontoxic concentrations of albiflorin and exposed to hydrogen peroxide (H₂O₂) to mimic oxidative stress. Albiflorin pretreatment inhibited H₂O₂-mediated decrease in cell viability and extracellular release of lactate dehydrogenase, and reduced comet tail formation, 8-hydroxy-2'-deoxyguanosine production, and phosphorylated form of histone 2AX expression, which are representative biomarkers of DNA damage. Albiflorin also blocked H₂O₂-induced apoptosis by inhibiting the activation of caspase-3, which is associated with the maintenance of mitochondrial membrane stability by decreasing the Bax/Bcl-2 expression ratio. Additionally, albiflorin markedly suppressed H₂O₂-induced accumulation of reactive oxygen species (ROS) and decreased glutathione levels, while increasing the phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2) and activating heme oxygenase-1 (HO-1) in the presence of H₂O₂. However, artificial inhibition of HO-1 activity using zinc protoporphyrin (ZnPP) markedly abrogated the protective effects of albiflorin against ROS production and mitochondrial damage in H₂O₂-treated cells. ZnPP significantly reversed the protective effects of albiflorin against H₂O₂-induced apoptosis and decreased cell viability. Taken together, these findings suggest that albiflorin protects myoblasts from oxidative stress-induced DNA damage and apoptosis by activating Nrf2/HO-1 signaling, thus highlighting its potential in the management of myofunctional homeostasis.

The present research work primarily investigated whether spinosin has the potential of improving the pathogenesis of Alzheimer's disease (AD) driven by β-amyloid (Aβ) overproduction through impacting the procession of amyloid precursor protein (APP). Wild type mouse Neuro-2a cells (N2a/WT) and N2a stably expressing human APP695 (N2a/APP695) cells were treated with spinosin for 24 h. The levels of APP protein and secreted enzymes closely related to APP procession were examined by western blot analysis. Oxidative stress related proteins, such as nuclear factor-erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) were detected by immunofluorescence assay and western blot analysis, respectively. The intracellular reactive oxygen species (ROS) level was analyzed by flow cytometry, the levels of Aβ_1-42 were determined by ELISA kit, and Thioflavin T (ThT) assay was used to detect the effect of spinosin on Aβ_1-42 aggregation. The results showed that ROS induced the expression of ADAM10 and reduced the expression of BACE1, while spinosin inhibited ROS production by activating Nrf2 and up-regulating the expression of HO-1. Additionally, spinosin reduced Aβ_1-42 production by impacting the procession of APP. In addition, spinosin inhibited the aggregation of Aβ_1-42. In conclusion, spinosin reduced Aβ_1-42 production by activating the Nrf2/HO-1 pathway in N2a/WT and N2a/APP695 cells. Therefore, spinosin is expected to be a promising treatment of AD.

Oxidative stress due to hyperglycemia damages the functions of retinal pigment epithelial (RPE) cells and is a major risk factor for diabetic retinopathy (DR). Paeoniflorin is a monoterpenoid glycoside found in the roots of Paeonia lactiflora Pall and has been reported to have a variety of health benefits. However, the mechanisms underlying its therapeutic effects on high glucose (HG)-induced oxidative damage in RPE cells are not fully understood. In this study, we investigated the protective effect of paeoniflorin against HG-induced oxidative damage in cultured human RPE ARPE-19 cells, an in vitro model of hyperglycemia. Pretreatment with paeoniflorin markedly reduced HG-induced cytotoxicity and DNA damage. Paeoniflorin inhibited HG-induced apoptosis by suppressing activation of the caspase cascade, and this suppression was associated with the blockade of cytochrome c release to cytoplasm by maintaining mitochondrial membrane stability. In addition, paeoniflorin suppressed the HG-induced production of reactive oxygen species (ROS), increased the phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2), a key redox regulator, and the expression of its downstream factor heme oxygenase-1 (HO-1). On the other hand, zinc protoporphyrin (ZnPP), an inhibitor of HO-1, abolished the protective effect of paeoniflorin against ROS production in HG-treated cells. Furthermore, ZnPP reversed the protective effects of paeoniflorin against HG-induced cellular damage and induced mitochondrial damage, DNA injury, and apoptosis in paeoniflorin-treated cells. These results suggest that paeoniflorin protects RPE cells from HG-mediated oxidative stress-induced cytotoxicity by activating Nrf2/HO-1 signaling and highlight the potential therapeutic use of paeoniflorin to improve the symptoms of DR.

Ginger, one of worldwide consumed dietary spice, is not only famous as food supplements, but also believed to exert a variety of remarkable pharmacological activity as herbal remedies. In this study, a ginger constituent, 12-dehydrogingerdione (DHGD) was proven that has comparable anti-inflammatory activity with positive control 6-shogaol in inhibiting LPS-induced interleukin (IL)-6, tumor necrosis factor $(TNF)-{\alpha}$, prostaglandin (PG) $E_2$, nitric oxide (NO), inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, without interfering with COX-1 in cultured microglial cells. Subsequent mechanistic studies indicate that 12-DHGD may inhibit neuro-inflammation through suppressing the LPS-activated $Akt/IKK/NF-{\kappa}B$ pathway. Furthermore, 12-DHGD markedly promoted the activation of NF-E2-related factor (Nrf)-2 and heme oxygenase (HO)-1, and we demonstrated that the involvement of HO-1 on the production of pro-inflammatory mediators such as NO and $TNF-{\alpha}$ by using a HO-1 inhibitor, Zinc protoporphyrin (Znpp). These results indicate that 12-DHGD may protect against neuro-inflammation by inhibiting $Akt/IKK/I{\kappa}B/NF-{\kappa}B$ pathway and promoting Nrf-2/HO-1 pathway.

Mutations in the luteinizing hormone/chorionic gonadotropin receptors (LH/CGRs), representatives of the G protein-coupled receptor family, have been rapidly identified over the last 20 years. This review aims to compare and analyze the data reported the activating and inactivating mutations of the LH/CGRs between human, rat, equine and fish, specifically (Japanese eel Anguilla japonica). Insights obtained through detailed study of these naturally-occurring mutations provide a further update of structure-function relationship of these receptors. Specifically, we present a variety of data on eel LH/CGR. These results provide important information about LH/CGR function in fish and the regulation of mutations of the highly conserved amino acids in glycoprotein hormone receptors.

Due to the COVID-19 pandemic situation, online education has emerged as an important research field to match its growing necessity. In this vein, this research explores one of the challenges facing online teaching of the Arabic language to Korean students at the university level based on the practical experience of online teaching in the academic year of 2020 while focusing on the role of students. The main goal of this research is to give some answers to its main question, which is: How is it possible to activate the role of students in the online classes of the Arabic language? The study suggests some online activities through which the role of students in online classes can be activated. An online survey questionnaire was provided to test the influence of some of those activities and to explore the students’ feedback. Additionally, interviews were conducted with some students to gain further understanding of their opinions about those activities. The results of the study showed positive feedback from the students towards those activities and provided some advantages of using those online activities for adding enjoyment to the students’ assignments. It is also recommended that teachers include more innovative online activities which match their students’ needs.