• Korean Journal of Head & Neck Oncology
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• v.27 no.1
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• pp.42-46
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• 2011

Background and Objectives : Serum stimulated thyroglobulin(stim Tg) was well-known for useful marker in detecting of recurrent or persistent papillary thyroid cancer after total thyroidectomy. Serum stim Tg level may be possibly related with recurrent tumor volume, but rarely studied. The purpose of this study was to examine the relationship between preoperative serum stim Tg level and recurrent tumor burden and to find additional clinical usefulness of stim Tg more than to detect a recurrence. Material and Methods : From January 2000 to December 2009, 40 patients who were operated due to neck recurrence of papillary thyroid cancer after total thyroidectomy were enrolled. All patients had preoperative stim Tg. We compared the clinical correlation of stim Tg and other variables to influence the preoperative stim Tg levels. Results : Preoperative stim Tg levels weren't correlated with site of recurrence, number of metastasis, maximal size, and presence of extra-capsular spread. But considerable increase of stim Tg more than 50ng/mL was identified in recurrence of lateral neck. Patients who have higher stim Tg level after surgery tend to be have higher preoperative stim Tg level. Conclusion : stim Tg was not elevated in 7.5% of recurrent PTC patients. Thus, other diagnostic modalities such as US may be important for these patients. If preoperative stim Tg was more than 50ng/mL, it may suggest recurrence in lateral neck and have less possibility to achieve postoperative biochemical remission.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.3
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• pp.343-348
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• 2018

Recent human genetic studies have shown that $G{\beta}5$ is related to various clinical symptoms, such as sinus bradycardia, cognitive disability, and attention deficit hyperactivity disorder. Although the calcium signaling cascade is closely associated with a heterotrimeric G-protein, the function of $G{\beta}5$ in calcium signaling and its relevance to clinical symptoms remain unknown. In this study, we investigated the in vitro changes of store-operated calcium entry (SOCE) with exogenous expression of $G{\beta}5$. The cells expressing $G{\beta}5$ had enhanced SOCE after depletion of calcium ion inside the endoplasmic reticulum. $G{\beta}5$ also augmented Stim1- and Orai1-dependent SOCE. An ORAI1 loss-of-function mutant did not show inhibition of $G{\beta}5$-induced SOCE, and a STIM1-ERM truncation mutant showed no enhancement of SOCE. These results suggested a novel role of GNB5 and Stim1, and provided insight into the regulatory mechanism of SOCE.

• The Journal of Korean Physical Therapy
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• v.21 no.2
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• pp.1-8
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• 2009

Purpose: This study examined the effect of EMG-stim related to the functional recovery of the upper extremity in chronic stroke patients with an intensive massed practice protocol. Methods: The subjects were assigned randomly to either the EMG-stim group (n=10) or sham treatment group (n=10). Both groups received conventional physical therapy, occupational therapy and FES, five times per week over a four week period. In the EMG-stim group, EMG-stim was applied to the hemiplegic wrist and finger extensors for 2 sessions for 30 minutes per day, 5 times per week over a 4 week period. As the pre- and the post-test, the following four motor tests were assessed as the function of the upper extremity clinical functional test: extensor digitorum strength test, Box and Block test, Fugl-Mayer Assessment, and Jebson-Taylor Hand Function Test. Results: In the Box and Block test and Fugl-Mayer Assessment, there were statistically significant differences between both groups as well as between pre- and post-test. The extensor digitorum and wrist extensor strength were similar in both groups. In the Jebson-Taylor Hand Function Test, there was a significant difference in simulated page turning but not in the other subtests. Conclusion: Intensive massed practice with EMG-stim intervention applied to the hemiplegic upper extremity is an effective therapeutic method for chronic stroke patients. However, a variety of intervention methods designed for stroke patients in clinical settings are needed.

• BMB Reports
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• v.51 no.8
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• pp.378-387
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• 2018

Skeletal muscle contracts or relaxes to maintain the body position and locomotion. For the contraction and relaxation of skeletal muscle, $Ca^{2+}$ in the cytosol of skeletal muscle fibers acts as a switch to turn on and off a series of contractile proteins. The cytosolic $Ca^{2+}$ level in skeletal muscle fibers is governed mainly by movements of $Ca^{2+}$ between the cytosol and the sarcoplasmic reticulum (SR). Store-operated $Ca^{2+}$ entry (SOCE), a $Ca^{2+}$ entryway from the extracellular space to the cytosol, has gained a significant amount of attention from muscle physiologists. Orai1 and stromal interaction molecule 1 (STIM1) are the main protein identities of SOCE. This mini-review focuses on the roles of STIM proteins and SOCE in the physiological and pathophysiological functions of skeletal muscle and in their correlations with recently identified proteins, as well as historical proteins that are known to mediate skeletal muscle function.

• Research in Community and Public Health Nursing
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• v.30 no.1
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• pp.47-56
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• 2019

Purpose: This study was performed to evaluate effects of a stim-up matt walking exercise program on balance and gait of the frail elderly. Methods: A total of 37 elderly people recruited from S city were randomly assigned to the experimental group (n=22) and control group (n=15). The stim-up matt walking exercise program was offered twice a week for 8 weeks. Data were analyzed by SPSS 21.0. Results: The dynamic balance ability Timed Up and Go test of the experimental group was significantly faster than that of the control group (t=21.72, p<.001). The static balance ability open-eye standing test (t=44.15, p<.001) and close-eye standing test (t=9.01, p=.005) also showed increase in effects of the experimental group. In the walking ability, gait cycle (t=2.48, p=.018), cadence (t=-2.21, p=.034) and gait speed (t=-2.78, p=.009), positive effects were on. However, no statistically significant differences were found in stride length and double support. At the ankle joint range left ankle plantar flexion (t=3.92, p<.001) and left ankle dorsal flexion (t=4.51, p<.001) were higher in the experimental group than in the control group, and also right ankle plantar flexion (t=2.79, p=.008) and right ankle dorsal flexion (t=2.92, p=.006) increased in the experimental group. Conclusion: The significance of this study is that the stim-up matt walking exercise program for the frail elderly proves to be useful for improving balance and walking.

• Journal of Ginseng Research
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• v.47 no.6
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• pp.755-765
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• 2023

Background: Caveolin-1, the scaffolding protein of cholesterol-rich invaginations, plays an important role in store-operated Ca²⁺ influx and its phosphorylation at Tyr14 (p-caveolin-1) is vital to mobilize protection against myocardial ischemia (MI) injury. SOCE, comprising STIM1, ORAI1 and TRPC1, contributes to intracellular Ca²⁺ ([Ca²⁺]_i) accumulation in cardiomyocytes. The purified extract of steamed Panax ginseng (EPG) attenuated [Ca²⁺]_i overload against MI injury. Thus, the aim of this study was to investigate the possibility of EPG affecting p-caveolin-1 to further mediate SOCE/[Ca²⁺]_i against MI injury in neonatal rat cardiomyocytes and a rat model. Methods: PP2, an inhibitor of p-caveolin-1, was used. Cell viability, [Ca²⁺]_i concentration were analyzed in cardiomyocytes. In rats, myocardial infarct size, pathological damages, apoptosis and cardiac fibrosis were evaluated, p-caveolin-1 and STIM1 were detected by immunofluorescence, and the levels of caveolin-1, STIM1, ORAI1 and TRPC1 were determined by RT-PCR and Western blot. And, release of LDH, cTnI and BNP was measured. Results: EPG, ginsenosides accounting for 57.96%, suppressed release of LDH, cTnI and BNP, and protected cardiomyocytes by inhibiting Ca²⁺ influx. And, EPG significantly relieved myocardial infarct size, cardiac apoptosis, fibrosis, and ultrastructure abnormality. Moreover, EPG negatively regulated SOCE via increasing p-caveolin-1 protein, decreasing ORAI1 mRNA and protein levels of ORAI1, TRPC1 and STIM1. More importantly, inhibition of the p-caveolin-1 significantly suppressed all of the above cardioprotection of EPG. Conclusions: Caveolin-1 phosphorylation is involved in the protective effects of EPG against MI injury via increasing p-caveolin-1 to negatively regulate SOCE/[Ca²⁺]_i.

• International Journal of Oral Biology
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• v.47 no.3
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• pp.33-40
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• 2022

Store-operated Ca²⁺ entry (SOCE) represents one of the major Ca²⁺ entry routes in non-excitable cells. It is involved in a variety of fundamental biological processes and the maintenance of Ca²⁺ homeostasis. The Ca²⁺ release-activated Ca²⁺ (CRAC) channel consists of stromal interaction molecule and Orai; however, the role and action of Homer proteins as an adaptor protein to SOCE-mediated Ca²⁺ signaling through the activation of CRAC channels in non-excitable cells still remain unknown. In the present study, we investigated the role of Homer2 in the process of Ca²⁺ signaling induced by the interaction between CRACs and Homer2 proteins in non-excitable cells. The response to Ca²⁺ entry by thapsigargin-mediated Ca²⁺ store depletion remarkably decreased in pancreatic acinar cells of Homer2^-/- mice, as compared to wild-type cells. It also showed critical differences in regulated patterns by the specific blockers of SOCE in pancreatic acinar cells of Homer2^-/- mice. The response to Ca²⁺ entry by the depletion in Ca²⁺ store markedly increased in the cellular overexpression of Orai1 and STIM1 as compared to the overexpression of Homer2 in cells; however, this response was remarkably inhibited by the overexpression of Orai1, STIM1, and Homer2. These results suggest that Homer2 has a critical role in the regulatory action of SOCE activity and the interactions between CRAC channels.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.1
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• pp.39-48
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• 2023

Spinal nerve injury causes mechanical allodynia and structural imbalance of neurotransmission, which were typically associated with calcium overload. Storeoperated calcium entry (SOCE) is considered crucial elements-mediating intracellular calcium homeostasis, ion channel activity, and synaptic plasticity. However, the underlying mechanism of SOCE in mediating neuronal transmitter release and synaptic transmission remains ambiguous in neuropathic pain. Neuropathic rats were operated by spinal nerve ligations. Neurotransmissions were assessed by whole-cell recording in substantia gelatinosa. Immunofluorescence staining of STIM1 with neuronal and glial biomarkers in the spinal dorsal horn. The endoplasmic reticulum stress level was estimated from qRT-PCR. Intrathecal injection of SOCE antagonist SKF96365 dose-dependently alleviated mechanical allodynia in ipsilateral hind paws of neuropathic rats with ED₅₀ of 18 ㎍. Immunofluorescence staining demonstrated that STIM1 was specifically and significantly expressed in neurons but not astrocytes and microglia in the spinal dorsal horn. Bath application of SKF96365 inhibited enhanced miniature excitatory postsynaptic currents in a dosage-dependent manner without affecting miniature inhibitory postsynaptic currents. Mal-adaption of SOCE was commonly related to endoplasmic reticulum (ER) stress in the central nervous system. SKF96365 markedly suppressed ER stress levels by alleviating mRNA expression of C/ EBP homologous protein and heat shock protein 70 in neuropathic rats. Our findings suggested that nerve injury might promote SOCE-mediated calcium levels, resulting in long-term imbalance of spinal synaptic transmission and behavioral sensitization, SKF96365 produces antinociception by alleviating glutamatergic transmission and ER stress. This work demonstrated the involvement of SOCE in neuropathic pain, implying that SOCE might be a potential target for pain management.

• The Korean Journal of Pain
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• v.29 no.1
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• pp.23-28
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• 2016

Background: Sacral nerve stimulation is a therapeutic option with demonstrated efficacy for conditions presenting with perineal pain caused by different etiologies. We aimed to assess whether a sacral electrode ($Interstim^{(R)}$, Medtronic, Minneapolis, MN, USA) inserted through the caudal pathway is able to offer an acceptable level of sacral stimulation and rate of catheter migration. Methods: We present 12 patients with pelvic pain who received sacral neuromodulation via the sacral hiatus with the InterStim electrode. We evaluated patient satisfaction as well as migration and removal of the electrode, if necessary. Results: Our experience included 12 patients, 10 women and two men, with a mean age of 60 years. In eight of the 12 patients, the initial therapy was effective, and the final system implantation was performed. During subsequent follow-up, patient satisfaction was good. To date, there have been no cases of electrode displacement or migration. Conclusions: The caudal insertion of the InterStim electrode, with its own fixation system, and initially designed for transsacral insertion, appears in our experience to be a satisfactory option which can minimize electrode displacements, achieving similar results in therapeutic efficacy and causing no difficulties in removal.

• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.371-379
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• 2016

Store-operated calcium entry (SOCE), a major mode of extracellular calcium entry, plays roles in a variety of cell activities. Accumulating evidence indicates that the intracellular calcium ion concentration and calcium signaling are critical for the responses induced by oxidative stress. The present study was designed to investigate the potential effect of SOCE inhibition on $H_2O_2$-induced apoptosis in endothelial progenitor cells (EPCs), which are the predominant cells involved in endothelial repair. The results showed that $H_2O_2$-induced EPC apoptosis was reversed by SOCE inhibition induced either using the SOCE antagonist ML-9 or via silencing of stromal interaction molecule 1 (STIM1), a component of SOCE. Furthermore, SOCE inhibition repressed the increases in intracellular reactive oxygen species (ROS) levels and endoplasmic reticulum (ER) stress and ameliorated the mitochondrial dysfunction caused by $H_2O_2$. Our findings provide evidence that SOCE inhibition exerts a protective effect on EPCs in response to oxidative stress induced by $H_2O_2$ and may serve as a potential therapeutic strategy against vascular endothelial injury.