• Korean Journal of Clinical Laboratory Science
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• v.37 no.3
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• pp.212-215
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• 2005

Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy in clinical practice, with a 0.1% life time risk in the general population. Conventional neurophysiological studies have been useful in the diagnosis of this condition, as have a number of more specialized procedures. Therefore, we evaluated the diagnostic sensitivities of several parameters in nerve conduction technique for CTS patients. We analyzed 100 patients (159 hands) who were diagnosed with CTS clinically and electrophysiolosically. Median motor and sensory nerve conduction velocities (MCV and SCV) with wrist, palm, and finger stimulation were performed in traditional methods. Sensitivities of each test were calculated and compared to normal control data. The sensitivities of existing nerve conduction method were noted in terminal latency on median nerve, 2nd finger-wrist segment, 3rd finger-wrist segment, palm-wrist segment and distoproximal ratio, as 72.96%, 92.45%, 94.34%, 94.97%, and 97.48%, respectively. In the early course of CTS, sensory nerve conductions in the median nerve are more valuable than motor nerve conduction. Sensory nerve conductions are usually affected before motor nerve conductions in CTS. In this study, we detected that slowing of median SCV was the most frequent in the distoproximal ratio.

• Annals of Clinical Neurophysiology
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• v.3 no.2
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• pp.128-135
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• 2001

Background : Tremor is uncommon manifestation of stroke. Therefore a few cases have been reported until now. There is still uncertainty about the characteristics of post-stroke tremor. Furthermore the pathogenesis and responsible structures of post-stroke tremor are not precisely known. We have recently experienced 34 cases of post-stroke tremor for the past 6 years. We analysed the clinical features and electrophysiologic findings of post-stroke tremor to evaluate the general characteristics and to analogize the possible pathogenetic mechanisms of post-stroke tremor. Methods : The clinical characteristics of post-stroke tremor were summarized in according to the onset time, involved body parts, types, tremor frequencies, neuroradiologic findings, and associated symptoms. The tremor frequencies were recorded by using a gyroscope. The spectral analysis of tremor frequencies were done automatically with Motus I soft ware. Results : Tremor onset were remarkably varied. Some patients showed a tremor appearing at the onset of a stroke and other patients showed delayed-onset tremor 10 years after a stroke. Tremor frequencies were also much varied. The range of hand tremor frequencies were from 1.5 to 12 Hz. Lesions were found in 31 cases(infarction 27, hemorrhage 4) on neuroimaging. In the cases of cerebral infarctions, 7 cases showed multiple small vessel diseases and 20 cases showed cerebral vessel lesions. The most commonly involved cerebral vessel lesion was the middle cerebral artery territory Several different clinical patterns of post-stroke tremor were identified. Conclusions : There are some evidences from the data summarized here to suggest that several pathogenetic mechanisms including central oscillators could be involved for the development of tremors and that tremor generating neural circuits could be more complex than previously suggested neural circuits.

• Journal of Korean Neurosurgical Society
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• v.39 no.3
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• pp.183-187
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• 2006

Objective : Hemifacial spasm has characteristic and specific electrophysiological finding, lateral spread response[LSR]. We study the correlation between change of lateral spread response during microvascular decompression[MVD] and clinical outcome after MVD. Methods : Sixty two patients with hemifacial spasm who were treated with microvascular decompression from March 2000 to February 2003 were included in this study. The monitoring of intraoperative facial electromyography[EMG] and brain stem auditory evoked potential were performed. Results : In 28 [44.7%] patients, there was persistence of lateral spread response after vascular decompression in root exit zone of facial nerve. Among these 28 patients, 9 had mild hemifacial spasm at discharge. Three out of 34 patients who had intraoperative disappearance of lateral spread response after MVD had mild hemifacial spasm. But Both groups, disappearance of LSR [Group I], and persistence [Group II] had only 2 patients with mild hemifacial spasm, and 5 patients at 3 months, respectively. Conclusion : Although intraoperative EMG monitoring is very useful in assessing the efficacy of MVD, the clinical outcome of MVD in patient with hemifacial spasm does not always correlate with EMG finding. The prognostic value of intraoperative LSR monitoring in the long-term results is questionable.

• Animal cells and systems
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• v.15 no.2
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• pp.131-138
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• 2011

Redox regulation is one of the ubiquitous mechanisms to modulate ion channels. We here investigated how 5,5'-dithio-bis (2-nitrobenzoic acid), a cysteine specific oxidizing reagent, modulates $Ca_v3.1$ and $Ca_v3.2$ T-type $Ca^{2+}$ channels expressed in Xenopus oocytes. Application of the reagent inhibited $Ca_v3.1$ and $Ca_v3.2$ currents in a dose-dependent manner. The oxidizing reagent (1 mM) reduced the peak amplitude of $Ca_v3.1$ and $Ca_v3.2$ currents by ~50% over 2-3 minutes and the decreased currents were fully recovered upon washout of it. The reagent slowed the activation and inactivation kinetics of $Ca_v3.1$, $Ca_v3.2$, and $Ca_v3.3$ channel currents. Notably, the reagent positively shifted both activation and steady-state inactivation curves of $Ca_v3.1$, while it did not those of $Ca_v3.2$. Utilizing chimeric channels from $Ca_v3.1$ and $Ca_v3.2$, we localized the domains III and IV of $Ca_v3.1$ responsible for the positive shifts of channel activation and steady-state inactivation. These findings provide hints relevant to the electrophysiological and molecular mechanisms accounting for the oxidative regulation of T-type channels.

• Animal Bioscience
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• v.34 no.5
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• pp.880-885
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• 2021

Objective: Omasum is an important site for the absorption of short chain fatty acids. The major route for the transport of acetate is via sodium hydrogen exchanger (NHE). However, a discrepancy in the symmetry of sodium and acetate transport has been previously reported, the mechanism of which is unclear. In this study, we investigated the possible role of carbonic anhydrase (CA) for this asymmetry. Methods: Omasal tissues were isolated from healthy sheep (N = 3) and divided into four groups; pH 7.4 and 6.4 alone and in combination with Ethoxzolamide. Electrophysiological measurements were made using Ussing chamber and the electrical measurements were made using computer controlled voltage clamp apparatus. Effect(s) of CA inhibitor on acetate and sodium transport flux rate of Na22 and 14C-acetate was measured in three different flux time periods. Data were presented as mean±standard deviation and level of significance was ascertained at p≤0.05. Results: Mucosal to serosal flux of Na (JmsNa) was greater than mucosal to serosal flux of acetate (JmsAc) when the pH was decreased from 7.4 to 6.4. However, the addition of CA inhibitor almost completely abolished this discrepancy (JmsNa ≈ JmsAc). Conclusion: The results of the present study suggest that the additional protons required to drive the NHE were provided by the CA enzyme in the isolated omasal epithelium. The findings of this study also suggest that the functions of CA may be exploited for better absorption in omasum.

• Journal of The Korean Society of Clinical Toxicology
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• v.19 no.2
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• pp.100-109
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• 2021

Purpose: The purpose of this study was to investigate effect of N-acetylcysteine (NAC) on the injury of putative parvalbumin positive interneurons defined by molecular marker and hippocampal long-term potentiation (LTP), a marker of neural plasticity following acute carbon monoxide (CO) poisoning. Methods: Adult Sprague-Dawley rats were exposed to 1100 ppm CO for 40 minutes followed by 3000 ppm CO for 20 minutes. Animals received daily intraperitoneal injection of NAC (150 mg/kg) for 5 days after CO exposure. Changes in learning and spatial memory were evaluated by Y-maze test 5 days after the poisoning. In vivo LTP in hippocampal CA1 area was evaluated by using extracellular electrophysiological technique. Immunohistochemical staining were adopted to observe expressional damages of parvalbumin (PV) immunoreactive interneurons in the hippocampus following the poisoning. Results: Acute CO intoxication resulted in no changes in memory performance at Y-maze test but a significant reduction of LTP in the in hippocampal CA1 area. There was also a significant reduction of PV (+) interneurons in the hippocampal CA1 area 5 days after CO poisoning. Daily treatment of NAC significantly improved hippocampal LTP impairment and reduced immunoreactivity for PV in the hippocampus following the acute CO poisoning. Conclusion: The results of this study suggest that reduction of hippocampal LTP and PV (+) interneurons in the hippocampus is sensitive indicator for brain injury and daily NAC injections can be the alternative therapeutics for the injury induced by acute CO poisoning.

• Genes and Genomics
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• v.40 no.12
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• pp.1269-1277
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• 2018

Bcl2-associated athanogene 3 (BAG3) mutations have been reported to cause the myofibrillar myopathy (MFM) which shows progressive limb muscle weakness, respiratory failure, and cardiomyopathy. Myopathy patients with BAG3 mutation are very rare. We described a patient showing atypical phenotypes. We aimed to find the genetic cause of Korean patients with sensory motor polyneuropathy, myopathy and rigid spine. We performed whole exome sequencing (WES) with 423 patients with sensory motor polyneuropathy. We found BAG3 mutation in one patient with neuropathy, myopathy and rigid spine syndrome, and performed electrophysiological study, whole body MRI and muscle biopsy on the patient. A de novo heterozygous p.Pro209Leu (c.626C>T) mutation in BAG3 was identified in a female myopathy. She first noticed a gait disturbance and spinal rigidity at the age of 11, and serum creatine kinase levels were elevated ninefolds than normal. She showed an axonal sensory-motor polyneuropathy like Charcot-Marie-Tooth disease (CMT), myopathy, rigid spine and respiratory dysfunction; however, she did not show any cardiomyopathy, which is a common symptom in BAG3 mutation. Lower limb MRI and whole spine MRI showed bilateral symmetric fatty atrophy of muscles at the lower limb and paraspinal muscles. When we track traceable MRI 1 year later, the muscle damage progressed slowly. As far as our knowledge, this is the first Korean patient with BAG3 mutation. We described a BAG3 mutation patient with atypical phenotype of CMT and myopathy, and those are expected to broaden the clinical spectrum of the disease and help to diagnose it.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.5
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• pp.357-366
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• 2019

$G{\alpha}_q$-coupled receptor stimulation was implied in the activation process of transient receptor potential canonical (TRPC)1/4 and TRPC1/5 heterotetrameric channels. The inactivation occurs due to phosphatidylinositol 4,5-biphosphate ($PI(4,5)P_2$) depletion. When $PI(4,5)P_2$ depletion was induced by muscarinic stimulation or inositol polyphosphate 5-phosphatase (Inp54p), however, the inactivation by muscarinic stimulation was greater compared to that by Inp54p. The aim of this study was to investigate the complete inactivation mechanism of the heteromeric channels upon $G{\alpha}_q$-phospholipase $C{\beta}$ ($G{\alpha}_q-PLC{\beta}$) activation. We evaluated the activity of heteromeric channels with electrophysiological recording in HEK293 cells expressing TRPC channels. TRPC1/4 and TRPC1/5 heteromers undergo further inhibition in $PLC{\beta}$ activation and calcium/protein kinase C (PKC) signaling. Nevertheless, the key factors differ. For TRPC1/4, the inactivation process was facilitated by $Ca^{2+}$ release from the endoplasmic reticulum, and for TRPC1/5, activation of PKC was concerned mostly. We conclude that the subsequent increase in cytoplasmic $Ca^{2+}$ due to $Ca^{2+}$ release from the endoplasmic reticulum and activation of PKC resulted in a second phase of channel inhibition following $PI(4,5)P_2$ depletion.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.5
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• pp.393-402
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• 2019

Aurora kinases inhibitors, including ZM447439 (ZM), which suppress cell division, have attracted a great deal of attention as potential novel anti-cancer drugs. Several recent studies have confirmed the anti-cancer effects of ZM in various cancer cell lines. However, there have been no studies regarding the cardiac safety of this agent. We performed several cytotoxicity, invasion and migration assays to examine the anti-cancer effects of ZM. To evaluate the potential effects of ZM on cardiac repolarisation, whole-cell patch-clamp experiments were performed with human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and cells with heterogeneous cardiac ion channel expression. We also conducted a contractility assay with rat ventricular myocytes to determine the effects of ZM on myocardial contraction and/or relaxation. In tests to determine in vitro efficacy, ZM inhibited the proliferation of A549, H1299 (lung cancer), MCF-7 (breast cancer) and HepG2 (hepatoma) cell lines with $IC_{50}$ in the submicromolar range, and attenuated the invasive and metastatic capacity of A549 cells. In cardiac toxicity testing, ZM did not significantly affect $I_{Na}$, $I_{Ks}$ or $I_{K1}$, but decreased $I_{hERG}$ in a dose-dependent manner ($IC_{50}$: $6.53{\mu}M$). In action potential (AP) assay using hiPSC-CMs, ZM did not induce any changes in AP parameters up to $3{\mu}M$, but it at $10{\mu}M$ induced prolongation of AP duration. In summary, ZM showed potent broad-spectrum anti-tumor activity, but relatively low levels of cardiac side effects compared to the effective doses to tumor. Therefore, ZM has a potential to be a candidate as an anti-cancer with low cardiac toxicity.

• Journal of Medicine and Life Science
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• v.15 no.2
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• pp.101-104
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• 2018

Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy caused by focal compression of the median nerve in the carpal tunnel. However, many patients with CTS, who are diagnosed clinically and confirmed with electrophysiological studies, complain of the sensory symptoms extends to the ulnar nerve territory. The aim of this study was to evaluate whether a dysfunction in sensory fibers of the ulnar nerve was present or not in hands with CTS patients who had extramedian spread of sensory symptoms over the hand. We retrospectively analyzed the recording of the subjects who were diagnosed with CTS within a one-year-period of time. After exclusions, 136 hands recordings of 87 patient were included. We compared the results of median and ulnar nerve sensory conduction studies between normal hands and hands with CTS. We did not detect statistically significant difference on all parameters of ulnar nerve sensory conduction studies between the normal hands and the hands with CTS. The parameters of the obtained in median nerve sensory conduction studies were statistically different between the healthy control and CTS patients. The hands with CTS showed similar rate of ulnar sensory conduction abnormalities compared with the normal hands. In conclusion, our study showed that none of the parameters in ulnar sensory nerve conduction studies differ between two groups. Accordingly, our study revealed that ulnar nerve involvement does not contribute in CTS patients underlying the spread of paresthesia extends to the ulnar nerve territory.