• Korean Journal of Clinical Laboratory Science
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• v.48 no.1
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• pp.41-48
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• 2016

Motor evoked potential of spinal surgery is known to cause damage due to the movement path of the continuous scan operation and surgery can be performed with minimized disability after surgery. However, if it is not at all formed at the wave motion evoked potential can occur during surgery and, in some cases the size of the waveform to be measured is very small and intermittent. In this case, the surgery cannot provide information about whether there is neurological damage. Increased intensity of the wave-induced motion of the dislocation does not occur if it appears in a very small amplitude stimulus, but changing the inspection area that electrical stimulation of the waveform changes could not be found. However, stimulation of a wide area in the cerebral cortex was found to occur with a waveform in the patients who underwent examination. Through this study, we propose a useful motor evoked potential test. From November to December 2015 three spine surgery patients visited Samsung Medical Center as neurosurgery patients with omission discomfort, gait disturbance, and no symptom of strength before surgery. In spine surgery patients with motor grade weakness, when motor evoked potential waveform has not been measured, in examination of the site of electrical stimulation of the cerebral cortex from entering the C3+C5/C4+C6 or C3+C1/C4+C2 if by the activity of more motor neuron unit, it was found that the waveform is better formed.

• The Journal of Korean Physical Therapy
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• v.24 no.6
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• pp.414-418
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• 2012

Purpose: Muscle fatigue affects proprioception, and it causes problems in spinal stability. The purpose of this study was to examine the effect on the accuracy of reproducing the lumbar angles before lumbar exercise and after fatiguing isokinetic lumbar exercise. Methods: Thirty healthy adults participated in this study. Before induction of fatigue by exercise, the proprioception was measured by Biodex. Lumbar positions were passively maintained on stimulation position ($25^{\circ}$ flexion and $25^{\circ}$ extension), and back to the starting position. Subjects actively repositioned the remembered stimulation position, and error degrees between the stimulation position and reposition were measured. Using an isokinetic device at $120^{\circ}$/sec of velocity of angle lumbar flexion/extension exercise resulted in muscle fatigue. The post-fatigue proprioceptive position sense was used in the same way as in pre-fatigue measurement. Results: Means of position sense of pre-fatigue were $2.19{\pm}1.97$ on flexion angle, and $5.04{\pm}2.84$ on extension angle. After exercise induced fatigue, means of position sense were $2.37{\pm}1.83$ on flexion angle, and $4.93{\pm}2.57$ on extension angle. Results of this study showed significant differences of lumbar proprioceptive position sense between pre- and post-fatigue. Conclusion: Lumbar proprioception sense in active repositioning in flexion and extension was affected in the presence of muscle fatigue. Therefore, it should be noted that therapeutic exercise for patients with abnormal proprioceptive sense or elderly people must be performed with care because muscle fatigue can cause secondary damage.

• Journal of Biomedical Engineering Research
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• v.36 no.4
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• pp.95-102
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• 2015

Epilepsy is a chronic neurological disease which produces repeated seizures. Over 30% of epileptic patients cannot be treated with anti-epileptic drugs, and surgical resection may cause loss of brain functions. Seizure suppression by electrical stimulation is currently being investigated as a new treatment method as clinical evidence has shown that electrical stimulation to brain could suppress seizure activity. In this paper, design of a real-time closed-loop neurostimulation system for epileptic seizure suppression is presented. The system records neural signals, detects seizures and delivers electrical stimulation. The system consists of a 6-channel electrode, front-end amplifiers, a data acquisition board by National Instruments, and a neurostimulator and Generic Osorio-Frei algorithm was applied for seizure detection. The algorithm was verified through simulation using electroencephalogram data, and the operation of whole system was verified through simulation and in- vivo test.

• Biomolecules & Therapeutics
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• v.10 no.3
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• pp.142-151
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• 2002

The present study was attempted to investigate the effect of apamin on catecholamine (CA) secretion evoked by ACh, high $K^+$, DMPP, McN-A-343, cyclopiazonic acid and Bay-K-8644 from the isolated perfused rat adrenal gland and to establish the mechanism of its action. The perfusion of apamin (1 nM) into an adrenal vein for 20 min produced greatly potentiation in CA secretion evoked by ACh (5.32 $ imes$ $10^{-3}$ M), high $K^+$, (5.6 $ imes$ $10^{-2}$), DMPP ($10^{-4}$ M for 2 min), McN-A-343 ($10^{-4}$ M for 2 min), cyclopiazonic acid ($10^{-5}$ M for 4 min) and Bay-K-8644 ($10^{-5}$ M for 4 min). However, apamin itself did fail to affect basal catecholamine output. Furthermore, in adrenal glands preloaded with apamin (1 nM) under the presence of glibenclamide ($10^{-6}$ M), an antidiabetic sulfonylurea that has been shown to be a specific blocker of ATP-regulated potassium channels (for 20 min), CA secretion evoked by DMPP and McN-A-343 was not affected. However, the perfusion of high concentration of apamin (100 nM) into an adrenal vein for 20 min rather inhibited significantly CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, cyclopiazonic acid and Bay-K-8644. Taken together, these results suggest that the low concentration of apamin causes greatly the enhancement of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization. These findings suggests that apamin-sensitive SK ($Ca^{2+}$) channels located in rat adrenal medullary chromaffin cells may play an inhibitory role in the release of catecholamines mediated by stimulation of cholinergic nicotinic and muscarinic receptors as well as membrane depolarization. However, it is thought that high concentration of apamin cause the inhibitory responses in catecholamine secretion evoked by stimulation of cholinergic receptors as well as by membrane depolarization from the rat adrenal gland without relevance with the SK channel blockade.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.148-149
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• 1998

It has been known that potassium channel openers are a new class of molecules that have attracted general interest because of their potent antihypertensive activity in vivo and vasorelaxant activity in vitro (Hamilton and Weston, 1989). In the present study, it was attempted to examine the effect of the potassium channel opener on catecholamine (CA) secretion evoked by cholinergic stimulation, membrane depolarization and calcium mobilization from the isolated perfused rat adrenal gland. The perfusion of pinacidil (30-300 uM) into an adrenal vein for 20 min produced relatively dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM), high $K^{+}$ (56 mM), DMPP (100 uM for 2 min), McN-A-343 (100 uM for 2 min), cyclopiazonic acid (10 uM for 4 min) and Bay-K-8644 (10 uM for 4 min). Also, under the presence of minoxidil (100 uM), which is also known to be a potassium channel activator, CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly depressed. However, in adrenal glands preloaded with pinacidil (100 uM) under the presence of glibenclamide (1 uM), an antidiabetic sulfonylurea that has been shown to be a specific blocker of ATP-regulated potassium channels (for 20 min), CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were considerably recovered to a considerable extent of the normal release as compared to that of pinacidil only. These results, taken together, suggest that pinacidil cause the marked inhibition of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization, indicating strongly that this effect may be mediated by inhibiting influx of extracellular calcium and release in intracellular calcium in the rat adrenomedullary chromaffin cells. Furthermore, these findings suggest strongly that these potassium channel openers-sensitive membrane potassium channels also play an important role in regulating CA secretion.

• Physical Therapy Rehabilitation Science
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• v.10 no.1
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• pp.76-81
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• 2021

Objective: Smartphone addiction can cause forward head posture, carpal tunnel syndrome and depression, and anxiety. Various interventions have been proposed to resolve Smartphone addiction. However, research regarding the efficacy of these interventions remains lacking. This study was conducted to investigate the effect of tDCS (Transcranial Direct Current Stimulation) on smartphone addiction solution and stress reduction. Design: A randomized controlled trial. Methods: The participants were divided randomly into two group (tDCS vs. Control). tDCS was applied to 41 adults (22.95±2.76 years). The tDCS group was applied 2 mA, for 13 minutes twice over a 26 minute period (n₁ = 21). The control (n₂ = 20) was not applied after padding and was applied twice for 13 minutes over a 26 minute period. This study was conducted four times a week for a total of four weeks. Results: Smartphone addiction for tDCS showed significant improvement in the results in the S-score (p<0.05, 95% CI: 0.702, 4.922), and the result of heart rate (HR) and skin conductivity (SC) to stress. The tDCS group and control group showed no significant decrese in the results in the HR (p>0.05, 95% CI: -3.390, 8.332), but tDCS group showed significant decrese in the results in the SC (p<0.05, 95% CI: 0.060, 1.343) Conclusions: This study suggected that smartphone addiction treatment and decreses of stress. The use of tDCS will reduce the addiction rate of adults and reduce stress, so that possible side effects in society can be solved.

• Journal of Acupuncture Research
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• v.23 no.4
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• pp.1-14
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• 2006

Objectives : We implemented the Moxa-Extract Moxibustion Method in order to improve the conventional moxibustion therapy. This method is aimed to eliminate burning wounds and smoke, which are the defects of conventional moxibustion therapy. And we performed to verify the efficiency by comparing the Moxa-Extract Moxibustion Method with the conventional Indirect Moxibustion Method. We measured the body heat and the lasting time of blood circulation improveent using thermography. We implemented the Moxa-Extract Moxibustion Method in order to improve the conventional moxibustion therapy. This method is aimed to eliminate burning wounds and smoke, which are the defects of conventional moxibustion therapy. And we performed to verify the efficiency by comparing the Moxa-Extract Moxibustion Method with the conventional Indirect Moxibustion Method. We measured the body heat and the lasting time of blood circulation improvement using thermography. Methods : The moxibustion therapy has two kinds of effects: The formers are pharmacological effects of the Moxa's vasodilators and antioxidants. The latters are thermal effects which cause improvement of the blood circulation. To remove the demerits without omission of above therapeutic effects, we extracted the vasodilators and antioxidant compounds from the Moxa-CH2Cl2 fraction Moxa-EtOA and composed the moxibustion kit with (Ba0.8 Sr0.2)0.996 Y0.004 TiO2 + 0.5WT SiO2% positive Temperature Coefficients Thermistor. The experimental demonstrations have been made by the stimulating the spot which is CV4(Kwan-Won), CV8(Shin-Guel), CV12(Jung-Wan) acupuncture points of the conception vessel meridian(CV). And stimulating time was one hour. We divided the subjects into 5 groups such as no stimulation group, conventional Indirect Moxibustion group, only Moxa-Extract stimulation group, only heat stimulation group, and Moxa-Extract Moxibustion group. In the different cases, we have measured the body heat in pre-stimulation, just after stimulation, 2 hours after, and 4 hours after. Results : he body heats of the group who were stimulated by the Moxa-Extract Moxibustion method were increased by over the $2^{\circ}C$. And the body heats of the group who were stimulated by the Indirect Moxibustion Method were increased by average the $1^{\circ}C$. We have evaluated that the Moxa-Extract Moxibustion Method is improvement on the Indirect Moxibustion Method by the increasing rate is 200% and increasing time is 150% with the body heat of the abdominal region. Conclusion : We have implemented the Moxa-Extract Moxibustion Method and evaluated the efficiency of the Moxa-Extract Moxibustion Method comparing with the Indirect Moxibustion Method.

• Korean Journal of Veterinary Research
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• v.35 no.2
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• pp.229-236
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• 1995

The effect of ${\alpha}_1$-adrenoceptor(${\alpha}_1$-AR) stimulation on intracellular pH($pH_i$), $Na^+$ activity($a_{Na}{^i}$) and contractility were investigated in isolated papillary muscles of euthyroid or hyperthyroid guinea pig with conventional microelectrode, $Na^+$ or $H^+$-selective microelectrodes, and tension transducer. Stimulation of the ${\alpha}_1$-AR by phenylephrine produced a decrease in $a_{Na}{^i}$ in euthyroid preparations. This decrease in $a_{Na}{^i}$ was abolished in presence of PKC activator, phorbol dibutyrate, and increased contrary to decrease. Phenylephrine also increased $a_{Na}{^i}$ in hyperthyroid ones. However, phenylrephtine produced an increase in $pH_i$ in both euthyroid and hyperthyroid ones. These changes were blocked by prazosin, an antagonist of ${\alpha}_1$-AR. These findings suggest that the changes in $a_{Na}{^i}$ and $pH_i$ are mediated by a stimulation of $Na^+-H^+$ exchange via ${\alpha}_1$-AR stimulation. This study focused on the increase in $a_{Na}{^i}$, $pH_i$ and contractility. The increase in $pH_i$ was blocked by amiloride or EIPA, $Na^+-H^+$ exchange inhibitors. Therefore, the increase in $a_{Na}{^i}$ and $pH_i$ mediated by ${\alpha}_1$-AR appeared to be due to an influx of $Na^+$ and a reduction of $H^+$ through $Na^+-H^+$ exchange. This study also revealed that the increase in $pH_i$ and $a_{Na}{^i}$ might be related to the sustained positive inotropic response. The $a_{Na}{^i}$ increase may contribute to the intracellular $Ca^{2+}$ through the $Na^+-Ca^{2+}$ exchange, and the $pH_i$ increase could cause an increase in the $Ca^{2+}$ sensitivity of myofilaments and may augment the ${\alpha}_1$-AR-mediated positive inotropic response.

• The Transactions of the Korean Institute of Electrical Engineers D
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• v.55 no.8
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• pp.386-396
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• 2006

We implemented the Drug-Pad Moxibustion Method in order to improve the conventional moxibustion therapy. This method is aimed to eliminate burning wounds and smoke, which are the defects of conventional moxibustion therapy. And we performed to verify the efficiency by comparing the Drug-Pad Moxibustion Method with the conventional Indirect Moxibustion Therapy. We measured the body heat and the lasting time of blood circulation improvement using thermography. The moxibustion therapy has two kinds of effects: The formers are pharmacological effects of the Moxa's vasodilators and antioxidants. The latters are thermal effects which cause improvement of the blood circulation. To remove the demerits without omission of above therapeutic effects, we extracted the vasodilators and antioxidant compounds from the Moxa-$CH_2Cl_2$ fraction Moxa-EtOAc and composed the moxibustion kit with $(Ba_{0.8}\;Sr_{0.2})_{0.996}\;Y_{0.004}\;TiO_2+0.5_{WT}\;SiO_2%$ Positive Temperature Coefficients Thermistor. The experimental demonstrations have been made by the stimulating the spot which is CV4(Kwan-Won), CV8(Shin-Guel), CV12(Jung-Wan) acupuncture points of the conception vessel meridian(CV). And stimulating time was one hour. We divided the subjects into 5 groups such as no stimulation group, conventional Indirect Moxibustion group, only Drug-Pad stimulation group, only heat stimulation group, and Drug-Pad Moxibustion group. In the different cases, we have measured the body heat in pre-stimulation, just after stimulation, 2 hours after, and 4 hours after. The body heats of the group who were stimulated by the Drug-Pad Moxibustion Method were increased by over the $2^{\circ}C$. And the body heats of the group who were stimulated by the Indirect Moxibustion Method were increased by average the $1^{\circ}C$. We have evaluated that the Drug-Pad Moxibustion Method is improvement on the conventional Indirect Moxibustion Method by the heat-increasing rate is 200% and the lasting time is 150% with the body heat of the abdominal region. In the conclusions, We have implemented the Drug-Pad Moxibustion Method and evaluated the efficiency of the Drug-Pad Moxibustion Method comparing with the conventional Indirect Moxibustion Method.

• BMB Reports
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• v.40 no.4
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• pp.467-474
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• 2007

Autosomal recessive polycystic kidney disease (ARPKD) is one of the important genetic disorders in pediatric practice. Mutation of the polycystic kidney and hepatic disease gene 1 (PKHD1) was identified as the cause of ARPKD. The gene encodes a 67-exon transcript for a large protein of 4074 amino acids termed fibrocystin, but its function remains unknown. The neoplastic-like in cystic epithelial proliferation and the epidermal growth factor/epidermal growth factor receptor (EGF/EGFR) axis overactivity are known as the most important characteristics of ARPKD. Since the misregulation of $Ca^{2+}$ signaling may lead to aberrant structure and function of the collecting ducts in kidney of rat with ARPKD, present study aimed to investigate the further mechanisms of abnormal proliferation of cystic cells by inhibition of PKHD1 expression. For this, a stable PKHD1-silenced HEK-293T cell line was established. Then cell proliferation rates, intracellular $Ca^{2+}$ concentration and extracellular signal-regulated kinase 1/2 (ERK1/2) activity were assessed after treatment with EGF, a calcium channel blocker and agonist, verapamil and Bay K8644. It was found that PKHD1-silenced HEK-293T cell lines were hyperproliferative to EGF stimulation. Also PKHD1-silencing lowered the intracellular $Ca^{2+}$ and caused EGF-induced ERK1/2 overactivation in the cells. An increase of intracellular $Ca^{2+}$ in PKHD1-silenced cells repressed the EGF-dependent ERK1/2 activation and the hyperproliferative response to EGF stimulation. Thus, inhibition of PKHD1 can cause EGF-induced excessive proliferation through decreasing intracellular $Ca^{2+}$ resulting in EGF-induced ERK1/2 activation. Our results suggest that the loss of fibrocystin may lead to abnormal proliferation in kidney epithelial cells and cyst formation in ARPKD by modulation of intracellular $Ca^{2+}$.