• 재활치료과학
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• 제3권2호
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• pp.49-57
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• 2014

목적 : 본 연구는 조산아를 대상으로 한 구강자극프로그램 실시가 구강식이수행에 영향을 미치는지를 알아보고자 하였다. 연구방법 : 연구대상은 조산 (25주)로 출생한 아동 1명이었으며, 총 4주간 연구를 진행하였다. 중재방법은 구강자극프로그램으로 뺨, 윗입술, 아랫입술, 윗입술과 아랫입술의 커브, 윗잇몸, 아랫잇몸, 뺨의 내부, 혀의 측면, 혀의 중간을 손가락으로 눌러주며 자극을 주는 9가지 활동으로 구성되었다. 구강식이수행 요인으로는 체중, 하루에 섭취하는 우유의 양, 한 번에 먹는 우유의 양, 한 번 우유 먹을 때 걸리는 시간으로 측정하였다. 각 요인은 매주, 시간에 따른 변화를 측정하였다. 결과 : 중재 실시 후, 대상자의 체중이 증가하였으며 하루에 먹는 우유의 양과 한 번에 먹는 우유의 양도 증가하였다. 한 번 우유를 먹을 때 걸리는 시간은 감소하였다. 결론 : 구강자극프로그램은 조산아의 구강식이 수행을 향상시킬 수 있는 방법이며, 따라서 가정과 치료환경에서 적절히 활용할 수 있을 것이다.

• 기본간호학회지
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• 제18권2호
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• pp.160-167
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• 2011

Purpose: The purpose of this study was to identify the effects of an oral stimulation program on premature infant's transition from tube feeding to bottle feeding, decrease in desaturation during feeding, and early discharge. Methods: This quasi-experimental study was performed in one neonatal intensive care unit (NICU) of an university hospital. The control group data (n=69) were obtained from June 2008 to May 2009, and the experimental group data (n=67), from June 2009 to May 2010. The oral stimulation program (OSP) was provided daily before feeding for the experimental group until transition to bottle feeding was completed. Results: The OSP group began bottle feeding earlier and were on complete bottle feeding earlier than control group. Discharge delay due to feeding desaturation was lower than for the control group. Conclusion: The results indicate that OSP for premature infants was helpful in transition from tube feeding to bottle feeding and early discharge and thus can contribute health and development in premature infants.

• International Journal of Oral Biology
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• 제31권3호
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• pp.87-92
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• 2006

Schwann cells play an important role in peripheral nerve regeneration. Upon nerve injury, Schwann cells are activated and produce various proinflammatory mediators including IL-6, LIF and MCP-1, which result in the recruitment of macrophages and phagocytosis of myelin debris. However, it is unclear how the nerve injury induces Schwann cell activation. Recently, it was reported that necrotic cells induce immune cell activation via toll-like receptors (TLRs). This suggests that the TLRs expressed on Schwann cells may recognize nerve damage by binding to the endogenous ligands secreted by the damaged nerve, thereby inducing Schwann cell activation. To explore the possibility, we stimulated iSC, a rat Schwann cell line, with damaged neuronal cell extracts (DNCE). The stimulation of iSC with DNCE induced the expression of various inflammatory mediators including IL-6, LIF, MCP-1 and iNOS. Studies on the signaling pathway indicate that $NF-{\kappa}B$, p38 and JNK activation are required for the DNCE-induced inflammatory gene expression. Furthermore, treatment of either anti-TLR3 neutralizing antibody or ribonuclease inhibited the DNCE-induced proinflammatory gene expression in iSC. In summary, these results suggest that damaged neuronal cells induce inflammatory Schwann cell activation via TLR3, which might be involved in the Wallerian degeneration after a peripheral nerve injury.

• 한국임상수의학회지
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• 제26권5호
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• pp.472-475
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• 2009

A 3-year old, female Cocker Spaniel dog was referred to Seoul National University Hospital for Animals with depression and vomiting. The dog was diagnosed as hypoadrenocorticism based on the typical electrolyte alteration and the result of adrenocorticotropic hormone (ACTH) stimulation test. Initial treatment with oral fludrocortisone at a dose rate of 0.02 mg/kg/q24h for 6 weeks period was ineffective at maintaining serum electrolyte concentrations within normal limits. Although a dose rate of oral fludrocortisone was significantly increased up to 0.06 mg/kg/q24h during 24 weeks period, the treatment was still ineffective. Moreover, the patient showed side effects related to the glucocorticoid excess including PU/PD, weight gain and lipemia. After alternation with desoxycorticosterone pivalate (DOCP, 2.2 mg/kg, IM) every 25 day, the clinical signs was disappeared and the electrolyte balance was maintain with no side effect. Therefore, DOCP may be suggested as an effective drug in canine hypoadrenocorticism uncontrolled with oral fludrocortisone.

• Journal of Oral Medicine and Pain
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• 제22권1호
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• pp.183-192
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• 1997

Pressure pain thresholds are routinely used in orofacial pain research to evaluate the response of deep orofacial tissues to mechanical stimulation. Like other psychophysical measurements, however, this technique must stimulate cutaneous tissues before stimulating deeper tissues. This study aimed at evaluating the influence of the cutaneous hypoesthesia on the pressure pain threshold in 30 healthy volunteers. PPTs were determined with electric pressure algometry over masseter, temporalis anterior, sternocleidomastoid, and trapezius muscle before and after skin hypoesthesia. A local anesthetic cream and a control cream were applied following a placebo-controlled double-blind design and PPTs were reassessed. Two examiners measured PPTs two times on each muscles, randomly. And the EMG activity of all muscles were measured to evaluate the relationship with PPTs. The collected data were processed by SAS/STAT program. The obtained results were as follows : 1. There were a tendency to increase PPTs after than before cutaneous hypoesthesia, but, there were no significant difference statistically. 2. PPTs were consistently higher in anterior temporalis than in masseter muscle. 3. In all occasions, PPTs were higher in males than in females(p<0.001). 4. A statistically significant correlation was obtained from values of intra-examiners and inter-examiners in all measured muscles. 5. A significantly positive correlation was not found between PPT and functional EMG activity.

• 근관절건강학회지
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• 제30권3호
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• pp.230-241
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• 2023

Purpose: This study aimed to verify the effects of a swallowing training program on swallowing function and depression for nursing home residents with dysphagia after stroke. Methods: This is a quasi-experimental study with non-equivalent control group pre-post test design. The program (oro-facial muscle strengthening exercises, swallowing exercises, expiratory muscle strengthening exercises, and brain stimulation exercises) applied to the experimental group three times per week for eight weeks, 40-45 minutes for each intervention. The final data from 42 people (21 experimental and 21 control) were analyzed by SPSS/WIN 25.0 using descriptive statistics. 𝜒² test, t-test, Wilcoxon rank sum test, and Friedman test. Results: The experimental group was significantly improved than control group in oro-facial muscle strength, swallowing symptoms (Z=-2.22, p=.026), and oral intake function level (Z=-2.00, p=.046). However, there was no significant difference between two groups in depression. Conclusion: This study is meaningful in that it reorganized and mediated a swallowing training program as a safe, non-invasive exercise that nurses can implement in a nursing facility with limited medical personnel and it could be easily followed by older adults.

• Molecules and Cells
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• 제38권9호
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• pp.796-805
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• 2015

Gintonin is a novel ginseng-derived lysophosphatidic acid (LPA) receptor ligand. Oral administration of gintonin ameliorates learning and memory dysfunctions in Alzheimer's disease (AD) animal models. The brain cholinergic system plays a key role in cognitive functions. The brains of AD patients show a reduction in acetylcholine concentration caused by cholinergic system impairments. However, little is known about the role of LPA in the cholinergic system. In this study, we used gintonin to investigate the effect of LPA receptor activation on the cholinergic system in vitro and in vivo using wild-type and AD animal models. Gintonin induced $[Ca^{2+}]_i $ transient in cultured mouse hippocampal neural progenitor cells (NPCs). Gintonin-mediated $[Ca^{2+}]_i $ transients were linked to stimulation of acetylcholine release through LPA receptor activation. Oral administration of gintonin-enriched fraction (25, 50, or 100 mg/kg, 3 weeks) significantly attenuated scopolamine-induced memory impairment. Oral administration of gintonin (25 or 50 mg/kg, 1 2 weeks) also significantly attenuated amyloid-${\beta}$ protein ($A{\beta}$)-induced cholinergic dysfunctions, such as decreased acetylcholine concentration, decreased choline acetyltransferase (ChAT) activity and immunoreactivity, and increased acetylcholine esterase (AChE) activity. In a transgenic AD mouse model, long-term oral administration of gintonin (25 or 50 mg/kg, 3 months) also attenuated AD-related cholinergic impairments. In this study, we showed that activation of G protein-coupled LPA receptors by gintonin is coupled to the regulation of cholinergic functions. Furthermore, this study showed that gintonin could be a novel agent for the restoration of cholinergic system damages due to $A{\beta}$ and could be utilized for AD prevention or therapy.

• Molecules and Cells
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• 제25권4호
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• pp.479-486
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• 2008

Mitogen-activated protein kinases (MAPKs) play an indispensable role in activation of the myogenic program, which is responsive to mechanical stimulation. Although there is accumulating evidence of mechanical force-mediated cellular responses, the role of MAPK in regulating the myogenic process in myoblasts exposed to cyclic stretch is unclear. Cyclic stretch induced the proliferation of C2C12 myoblasts and inhibited their differentiation into myotubes. In particular, it induced persistent phosphorylation of p38 kinase, and decreased the level of phosphorylation of extracellular-signal regulated kinase (ERK). Partial inhibition of p38 phosphorylation increased cellular levels of MyoD and p-ERK in stretched C2C12 cells, along with increased myotube formation. Treatment with $10{\mu}M$ PD98059 prevented myogenin expression in response to a low dose of SB203580 ($3{\mu}M$) in the stretched cells, suggesting that adequate ERK activation is also needed to allow the cells to differentiate into myotubes. These results suggest that cyclic stretch inhibits the myogenic differentiation of C2C12 cells by activating p38-mediated signaling and inhibiting ERK phosphorylation. We conclude that p38 kinase, not ERK, is the upstream signal transducer regulating cellular responses to mechanical stretch in skeletal muscle cells.