Kim, Hyunjoong;Song, Seonghyeok;Lee, Sangbong;Lee, Seungwon
Physical Therapy Rehabilitation Science
/
v.10
no.1
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pp.1-9
/
2021
Objective: Joint mobilization for arthrokinematics altered by the positional fault of chronic ankle instability (CAI) is an effective intervention for stabilization. In this study, we compared the effects of ankle dorsi flexion range of motion (DFROM) and dynamic balance ability (DBA) in CAI patients via passive joint mobilization (PJM), a method traditionally performed in previous studies, and active joint mobilization (AJM), a method that can have a greater effect on cortical excitability with spontaneous movements. Design: Single-blind two-arm randomized controlled trial Methods: A total of 30 participants were registered: 15 each to the PJM and AJM groups. Each participant received a total of 10 intervention sessions, 10 minutes per session, 5 times a week for 2 weeks. PJM used Maitland's mobilization method to apply joint mobilization with talus in the posterior direction and AJM used an angular joint motion to induce patient's voluntary motion of medial malleolus anterior gliding and lateral malleolus posterior gliding, respectively. DFROM of the ankle was measured by using tape and DBA was evaluated by using the balance system. Results: Significant improvement was observed after intervention in both the PJM and AJM groups except for the DBA-anterior and DBA-right variables of the PJM group. There were statistically significant differences between the AJM and PJM groups in the DFROM, DBA-anterior, DBA-posterior, and DBA-right variables. Conclusions: The overall improvement of DFROM and DBA was found to be more effective in joint mobilization including voluntary movement. When it is accompanied by voluntary movement, it further affects the neuromuscular system of the ankle.
Ethanol often causes critical health problems by altering the neuronal activities of the central and peripheral nerve systems. One of the cellular targets of ethanol is the plasma membrane proteins including ion channels and receptors. Recently, we reported that ethanol elevates membrane excitability in sympathetic neurons by inhibiting Kv7.2/7.3 channels in a cell type-specific manner. Even though our studies revealed that the inhibitory effects of ethanol on the Kv7.2/7.3 channel was diminished by the increase of plasma membrane phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), the molecular mechanism of ethanol on Kv7.2/7.3 channel inhibition remains unclear. By investigating the kinetics of Kv7.2/7.3 current in high K+ solution, we found that ethanol inhibited Kv7.2/7.3 channels through a mechanism distinct from that of tetraethylammonium (TEA) which enters into the pore and blocks the gate of the channels. Using a non-stationary noise analysis (NSNA), we demonstrated that the inhibitory effect of ethanol is the result of reduction of open probability (PO) of the Kv7.2/7.3 channel, but not of a single channel current (i) or channel number (N). Finally, ethanol selectively facilitated the kinetics of Kv7.2 current suppression by voltage-sensing phosphatase (VSP)-induced PI(4,5)P2 depletion, while it slowed down Kv7.2 current recovery from the VSP-induced inhibition. Together our results suggest that ethanol regulates neuronal activity through the reduction of open probability and PI(4,5)P2 sensitivity of Kv7.2/7.3 channels.
Objectives: This study was designed to investigate the difference between genuine and pseudo-halitosis in terms of clinical characteristics. Methods: We recruited 51 halitosis patients who visited the halitosis clinic at Kyung Hee University Korean Medicine Hospital from March 2020 to March 2022. We classified the halitosis patients into two groups, genuine and pseudo halitosis, based on oral chroma and evaluated the status of hyposalivation using the drainage method, stress levels using heart rate variability (HRV) parameters, and Ryodoraku. Results: Comparing the genuine halitosis group and the pseudo halitosis group, there was no significant difference in the status of hyposalivation and HRV parameters. However, Ryodoraku was significantly different between genuine and pseudo halitosis. Compared to the genuine halitosis group, the pseudo halitosis group showed a significantly higher value of total average (TA) of Ryodoraku. Conclusion: The results of this study suggest that there is a significant difference in Ryodoraku between genuine halitosis and pseudo halitosis, so when approaching pseudo halitosis patients, we should consider their excitability of the sympathetic nervous system and metabolic function status.
Background: The gastrocnemius tightness can easily occur. Gastrocnemius tightness results in gait disturbance. Thus, various interventions have been used to release a tight gastrocnemius muscle and improve gait performance. Moreover, focal muscle vibration (FMV) has recently been extensively researched in terms of tight muscle release and muscle performance. However, no study has investigated the effects of FMV application on medial gastrocnemius architectural changes. Objects: In this study, we aimed to investigate the effects of FMV on medial gastrocnemius architecture in persons with limited ankle dorsiflexion. Methods: Thirty one persons with <10° of passive ankle dorsiflexion participated in this study. We excluded persons with acute ankle injury within six months prior to study onset, a history of ankle fracture, leg length discrepancy greater than 2 cm, no history of neurological dysfunction, or trauma affecting the lower limb. The specifications of the FMV motor were as follows: a fixed frequency (fast wave: 150 Hz) and low amplitude (0.3-0.5 mm peak to peak) of vibration; the motor was used to release the medial gastrocnemius for 15 minutes. Each participant completed three trials for 10 days; a 30-second rest period was provided between each trial. Medial gastrocnemius architectural parameters [muscle thickness (MT), fiber bundle length (FBL), and pennation angle (PA)] were measured via ultrasonography. Results: MT significantly decreased after FMV application (p < 0.05). FBL significantly increased from its baseline value after FMV application (p < 0.05). PA significantly decreased from its baseline value after FMV application (p < 0.05). Conclusion: FMV application may be advantageous in reducing medial gastrocnemius excitability following a decrease in the amount of contractile tissue. Furthermore, FMV application can be used as a stretching method to alter medial gastrocnemius architecture.
Ji Seon Yang;Hyun-Jong Jang;Ki-Wug Sung;Duck-Joo Rhie;Shin Hee Yoon
The Korean Journal of Physiology and Pharmacology
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v.28
no.5
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pp.413-422
/
2024
Group I metabotropic glutamate receptors (mGluRs) modulate postsynaptic neuronal excitability and epileptogenesis. We investigated roles of group I mGluRs on low extracellular Mg2+ concentration ([Mg2+]o)-induced epileptiform activity and neuronal cell death in the CA1 regions of isolated rat hippocampal slices without the entorhinal cortex using extracellular recording and propidium iodide staining. Exposure to Mg2+-free artificial cerebrospinal fluid can induce interictal epileptiform activity in the CA1 regions of rat hippocampal slices. MPEP, a mGluR 5 antagonist, significantly inhibited the spike firing of the low [Mg2+]o-induced epileptiform activity, whereas LY367385, a mGluR1 antagonist, did not. DHPG, a group 1 mGluR agonist, significantly increased the spike firing of the epileptiform activity. U73122, a PLC inhibitor, inhibited the spike firing. Thapsigargin, an ER Ca2+-ATPase antagonist, significantly inhibited the spike firing and amplitude of the epileptiform activity. Both the IP3 receptor antagonist 2-APB and the ryanodine receptor antagonist dantrolene significantly inhibited the spike firing. The PKC inhibitors such as chelerythrine and GF109203X, significantly increased the spike firing. Flufenamic acid, a relatively specific TRPC 1, 4, 5 channel antagonist, significantly inhibited the spike firing, whereas SKF96365, a relatively non-specific TRPC channel antagonist, did not. MPEP significantly decreased low [Mg2+]o DMEM-induced neuronal cell death in the CA1 regions, but LY367385 did not. We suggest that mGluR 5 is involved in low [Mg2+]o-induced interictal epileptiform activity in the CA1 regions of rat hippocampal slices through PLC, release of Ca2+ from intracellular stores and PKC and TRPC channels, which could be involved in neuronal cell death.
It is well known that extracellular Calcium plays a very important role in several steps of smooth muscle excitability and contractility, and there have been many concerns about factors influencing the distribution of extracellular Ca++ and the Ca++ flux through the cell membrane of the smooth muscle. Based on the assumption that Mg++ may also play an important role in the excitation and contraction processes of the smooth muscle by taking part in affecting Ca++ distribution and flux, many researches are being performed about the exact role of Mg++, especially in the vascular smooth muscle. But yet the effect of Mg++ in the smooth muscle activity is not clarified, and moreover the mechanism of Mg++ action is almost completely unknown. Present study attempted to clarify the effect of Mg++ on the excitability and contractility in the multiunit and unitary smooth muscle, and the mechanism concerned in it. The preparations used were the guinea-pig aortic strip as the experimental material of the multiunit smooth muscle and the rat uterine strip as the one of the unitary smooth muscle. The tissues were isolated from the sacrificed animal and were prepared for recording the isometric contraction. The effects of Mg++ and Ca++ were examined on the electrically driven or spontaneous contraction of the preparations. And the effects of these ions were also studied on the K+ or norepinephrine contracture. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% 02 and kept at 35oC. The results obtained were as follows: 1] Mg++ suppressed the phasic contraction induced by electrical field stimulation dose-dependently in the guinea-pig aortic strip, while the high concentration of Ca++ never recovered the decreased tension. These phenomena were not changed by the a - or b - adrenergic blocker. 2]Mg++ played the suppressing effect on the low concentration [20 and 40 mM] of K+-contracture in the aortic muscle, but the effect was not shown in the case of 100mM K+-contracture. 3] Mg++ also suppressed the contracture induced by norepinephrine in the aortic preparation. And the effect of Mg++ was most prominent in the contracture by the lowest [10 mM] concentration of norepinephrine. 4] In both the spontaneous and electrically driven contractions of the uterine strip, Mg++ decreased the amplitude of peak tension, and by the high concentration of Ca++ the amplitude of tension was recovered unlike the aortic muscle. 5] The frequency of the uterine spontaneous contraction increased as the [Ca++] / [Mg++] ratio increased up to 2, but the frequency decreased above this level. 6] Mg++ decreased the tension of the low[20 and 40mM] K+-contracture in the uterine smooth muscle, but the effect did not appear in the 100mM K+-contracture. From the above results, the following conclusion could be made. 1] Mg++ seems to suppress the contractility directly by acting on the smooth muscle itself, besides through the indirect action on the nerve terminal, in both the aortic and uterine smooth muscles. 2] The fact that the depressant effect of Mg++ on the K+-contracture is in inverse proportion to an increase of K+ concentration appears resulted from the extent of the opening state of the Ca++ channel. 3] Mg++ may play a depressant role on both the potential dependent and the receptor-operated Ca++ channels. 4] The relationship between the actions of Mg++ and Ca++ seems to be competitive in uterine muscle and non-competitive in aortic strip.
Excessive influx and the subsequent rapid cytosolic elevation of $Ca^{2+}$ in neurons is the major cause to induce hyperexcitability and irreversible cell damage although it is an essential ion for cellular signalings. Therefore, most neurons exhibit several cellular mechanisms to homeostatically regulate cytosolic $Ca^{2+}$ level in normal as well as pathological conditions. Delayed rectifier $K^+$ channels ($I_{DR}$ channels) play a role to suppress membrane excitability by inducing $K^+$ outflow in various conditions, indicating their potential role in preventing pathogenic conditions and cell damage under $Ca^{2+}$-mediated excitotoxic conditions. In the present study, we electrophysiologically evaluated the response of $I_{DR}$ channels to hyperexcitable conditions induced by high $Ca^{2+}$ pretreatment (3.6 mM, for 24 hours) in cultured hippocampal neurons. In results, high $Ca^{2+}$-treatment significantly increased the amplitude of $I_{DR}$ without changes of gating kinetics. Nimodipine but not APV blocked $Ca^{2+}$-induced $I_{DR}$ enhancement, confirming that the change of $I_{DR}$ might be targeted by $Ca^{2+}$ influx through voltage-dependent $Ca^{2+}$ channels (VDCCs) rather than NMDA receptors (NMDARs). The VDCC-mediated $I_{DR}$ enhancement was not affected by either $Ca^{2+}$-induced $Ca^{2+}$ release (CICR) or small conductance $Ca^{2+}$-activated $K^+$ channels (SK channels). Furthermore, PP2 but not H89 completely abolished $I_{DR}$ enhancement under high $Ca^{2+}$ condition, indicating that the activation of Src family tyrosine kinases (SFKs) is required for $Ca^{2+}$-mediated $I_{DR}$ enhancement. Thus, SFKs may be sensitive to excessive $Ca^{2+}$ influx through VDCCs and enhance $I_{DR}$ to activate a neuroprotective mechanism against $Ca^{2+}$-mediated hyperexcitability in neurons.
Journal of the korean academy of Pediatric Dentistry
/
v.30
no.3
/
pp.341-347
/
2003
Smith-Magenis syndrome (SMS) is a clinically recognizable multiple congenital anomaly and mental retardation syndrome caused by an interstitial deletion of chromosome 17 p11.2. Physical features include short stature, characteristic facial appearance: flattened mid-face, down-turned mouth, prominent and often rosy cheeks; prominent jaw in older children and adults, chronic ear infections, hearing impairment, eye problems, including: strabismus (an eye which turns in or out) and myopia (nearsightedness), hoarse voice, short fingers and toes, heart defects or murmurs, problems related to the urinary system, scoliosis (curvature of the spine), an unusual gait (walking pattern), and decreased sensitivity to pain. Behavioral and developmental characteristics include speech delay and articulation problems, developmental delay, learning disability, mental retardation, hyperactivity, self-injury, including: head banging; hand biting; picking at skin, sores and nails; pulling off finger- and toenails; inserting foreign objects into ears, nose, or other body orifices, explosive outbursts, prolonged tantrums, destructive and aggressive behavior, excitability, arm hugging or hand squeezing when excited. This report is the case of a Korean 3-year-3-month old male with Smith-Magenis syndrome referred from local clinic for the treatment of dental caries. The patient was treated by physical restraint after prophylatic administration of antibiotic(Amoxacillin 50mg/kg).
Kim, Shin Tae;Kim, Hae Won;Kim, Se Joo;Kang, Jee In
Korean Journal of Biological Psychiatry
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v.24
no.3
/
pp.95-109
/
2017
Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive neuromodulation technique which can change cortical excitability in targeted area by producing magnetic field pulses with an electromagnetic coil. rTMS treatment has been used to treat various neuropsychiatric disorders including depression. In this review, we evaluate the literature on rTMS for depression by assessing its efficacy on different subtypes of depression and different technical parameters. In particular, we focus on the results of randomized clinical trials and meta-analyses for depression after the US Food and Drug Administration approval in 2008, which acknowledged its efficacy and acceptability. We also review the new forms of rTMS therapy including deep TMS, theta-burst stimulation, and magnetic seizure therapy (MST) that have been under recent investigation. High frequency rTMS over left dorsolateral prefrontal cortex (DLPFC), low frequency rTMS over right DLPFC, or bilateral rTMS is shown to be effective and acceptable in treatment for patients with non-psychotic, unipolar depression either as monotherapy or adjuvant. Deep TMS, theta-burst stimulation and MST are promising new TMS techniques which warrant further research.
Zinc is an endogenous transition metal that can be synaptically released during neuronal activity. However, zinc may contribute to the neuropathology associated with a variety of conditions. Carnosine expressed in glial cells can modulate the effects of zinc on neuronal excitability as a zinc chelator. We hypothesize that carnosine may protect against neurotoxicity of zinc in cortical neuronal cells. The cortical neuronal cells from newborn rats were prepared and exposed to zinc chloride and/or carnosine at various concentrations. Zinc at the doses of 0 to $500{\mu}M$ decreased neuronal cell viability in a dose-dependent manner. Additionally, at the concentrations of 100 and $200{\mu}M$, it significantly decreased cell viability in an exposed time-dependent manner (p < 0.05). Treatment with carnosine at the concentrations of 20 and $200{\mu}M$ significantly increased neuronal cell proliferation by approximately 14% and 20%, respectively, compared to the control (p < 0.05). At the concentrations of 100 and $200{\mu}M$ zinc, $20{\mu}M$ carnosine significantly increased the viability of neuronal cells by 18.3% and 12.1 %, and $200{\mu}M$ carnosine also increased it by 33.5% and 28.6%, respectively, compared to the normal control group (p < 0.01). These results suggest that carnosine at a physiologically relevant level may protect against zinc-mediated toxicity in neuronal cells as an endogenous neuroprotective agent.
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