Earticle

Objective: In current urodynamic studies, rectal catheters can cause erroneous result affecting detrusor pressure, and the catheter itself is not comfortable to the patients. To reduce these problems we investigated the relationship between the motor unit action potentials (MUAP) of rectus abdominis muscle and the abdominal pressure measured by rectal catheter. Method: Healthy seven men and three women volunteers (mean age: 49 years) with no neurological abnormality were enrolled. Possible maximal abdominal pressure (Pmax) was attained by Valsalva maneuver for 5 seconds. The MUAPs of the rectus abdominis muscle were recorded with surface electrodes for analysis. These recordings were done on 100, 80, 60, 40, and 20% of Pmax. The parameters of MUAP such as mean frequency, median frequency, turns, mean amplitude, and RMS (root mean square) were measured. Results: Turns, mean amplitude, and RMS　were increased in a proportion to the increment of abdominal pressure in all subjects (R=0.840, 0.879, and 0.984, respectively). Conclusion: These findings suggested that the surface MUAP of rectus abdominis muscle might be used indirectly for more convenient measurement of the abdominal pressure.

Objective: To compare the sensory nerve action potentials (SNAPs) between patients with cervical 6-7 foraminal stenosis (FS) and those without. Methods: We enrolled patients who underwent a bilateral nerve conduction study (NCS) between January 2016 and December 2017. The FS group (n=35) included patients whose lesion was located at C6-7 FS. The non-FS group (n=75) had no lesions at C6-7 foramen. The amplitudes and latencies of SNAPs on the affected side were compared between the two groups. The proportion of those with abnormal SNAP responses was also evaluated. Results: Compared with the non-FS group, the FS group had a significantly lower amplitude (30.5 vs. 40.2 AV; age-adjusted p<0.001) and a longer latency (3.31 vs. 3.17 ms; age-adjusted p=0.001) of the median nerve. Abnormal amplitude was observed in 20.0% of the FS group and 4.0% of the non-FS group (age-adjusted p=0.007), and abnormal latency was observed in 45.7% of the FS group and 26.7% of the non-FS group (age-adjusted p=0.010). The median SNAP ratio between the affected side and the unaffected side was not significantly different between the two groups. Conclusion: Patients with C6-7 FS had a lower amplitude and a longer latency of the median nerve than did those without. Abnormal SNAP amplitude and latency were significantly more common in patients with FS. SNAP amplitude may be used as a predictor of cervical FS.

본 연구는 감정의 이동이나 발생과정을 알아 문학치료에 활용하고자 하는 데에 목적이 있다. 그래서 문학작품 을 대할 때 인체에서 작동되는 감정의 유로에 대한 과정을 밝혀보고자 하였다. 그 결과 감정은 시어들을 읊을 때 인 체에서 감정 코드들이 작동하여 서로 끌어당겨 아미노산의 위치로 집결됨을 확인하였다. 그러면서 아미노산의 합성에 촉매 역할을 하는 것이 감정이라고 판단되었다. 물론 이는 인문학적이고 융합적인 논증이며, 의학적으로 증명된 사실 은 아니다. 그러나, 이러한 연구가 계속된다면 인간을 보다 건강하게 사유케 하는 데에 기여할 것으로 사료된다.

The purpose of this study is to utilize emotional movement and developmental process in literary therapy. So, I tried to reveal the process of the emotional channel that works in the human body when we deal with literary works. As a result, the emotions confirmed that the emotional codes in the human body were pulled from each other and gathered to the positions of amino acids when the shears were spoken. However, it was judged emotionally to act as a catalyst for the synthesis of amino acids. Of course, this is a humanistic and convergent argument, not a medical proof. However, if these studies continue, it will contribute to making people think more healthily.

Background and Purpose Acetylcholinesterase inhibitors (AChEIs) are widely used to treat myasthenia gravis (MG). Although AChEIs are usually tolerated well, some MG patients suffer from side effects. Furthermore, a small proportion of MG patients show cholinergic hy-persensitivity and cannot tolerate AChEIs. Because repetitive compound muscle action poten￢tials (R-CMAPs) are an electrophysiologic feature of cholinergic neuromuscular hyperactivi￢ty, we investigated the clinical characteristics of MG patients with R-CMAPs to identify their clinical usefulness in therapeutic decision-making. Methods We retrospectively reviewed the clinical records and electrodiagnostic findings of MG patients who underwent electrodiagnostic studies and diagnostic neostigmine testing (NT). Results Among 71 MG patients, 9 could not tolerate oral pyridostigmine bromide (PB) and 17 experienced side effects of PB. R-CMAPs developed in 24 patients after NT. The high￢est daily dose of PB was lower in the patients with R-CMAPs (240 mg/day vs. 480 mg/day, p<0.001). The frequencies of PB intolerance and side effects were higher in the patients with R-CMAPs than in those without R-CMAPs [37.5% vs. 0% (p<0.001) and 45.8% vs. 12.8% (p=0.002), respectively]. The MG Foundation of America postintervention status did not dif￢fer significantly between MG patients with and without R-CMAPs, and the response to im￢munotherapy was also good in both groups. Conclusions Side effects of and intolerance to AChEIs are more common in MG patients with R-CMAPs than in those without R-CMAPs. AChEIs should be used carefully in MG pa￢tients with R-CMAPs. The presence of R-CMAPs after NT may be a good indicator of the risks of PB side effects and intolerance.

The purpose of this study was to determine whether the effects of the superoxide donor menadione on myocardial electrical activity were regional and/or age-dependent. Action potentials were recorded in cardiac muscles that were isolated from 18- and 49-day old rat hearts, using a conventional microelectrode technique. Superoxide dismutase (SOD) activity was determined spectrophotometrically in regional cardiac muscles. Menadione (30 ${\mu}M$) significantly increased the action potential duration at 90% repolarization ($APD_{90}$) in Purkinje fibers and ventricular muscles from 18-day old rats; and it decreased the APD in ventricular muscles from 49-day old rats. ATP-sensitive $K^+$ ($K_{ATP}$) channel opener pinacidil blocked menadione-induced effects on the $APD_{90}$ of Purkinje fibers and ventricular muscles from 18-day old rats, but did not block menadione-induced effects on the $APD_{90}$ of Purkinje fibers and ventricular muscles from 49-day old rats. The cGMP-dependent protein kinase (PKG) activator or inhibitor did not inhibit the menadione-induced effects on $APD_{90}$ of ventricular muscles and Purkinje fibers from 18-and 49-day old rats. The superoxide dismutase (SOD) activities in ventricular muscles from 4-, 18- and 49-day old rats, were: 1185 ${\pm}$ 135, 1434 ${\pm}$ 96, and 1760 ${\pm}$ 144 U/mg protein, respectively; whereas, the SOD activities in atrial muscles, were: 1135.4 ${\pm}$ 156.4, 1145.4 ${\pm}$ 148.8, and 1243.5 ${\pm}$ 175.2 U/mg protein, respectively. However, the ventricular SOD activities were significantly inhibited under hypoxic conditions. These results indicate that menadione can produce regionally differential effects on cardiac APD, which may be due to differences in the SOD activity, depending on the region and age of the cardiac tissue.

Volume-regulated anion channels (VRACs) and TMEM16A calcium-activated chloride channels (CaCCs) are distinct but share some features and can co-immunoprecipitate. Currently, there are no specific inhibitors for these channels exist. Our prior research showed Flavoxate inhibits VRAC currents in HEK293 cells under hypotonic conditions. MFCA (3-methylflavone-8-carboxylic acid, a primary active metabolite of Flavoxate) and 3-methylflavone are two structural analogues of Flavoxate. To further elucidate the specific inhibitory effects of the three flavonoids on VRACs and TMEM16A/CaCCs, the current study used patch-clamp techniques to explore their effects on the two chloride channels. Additionally, we investigated the effects of the three flavonoids on action potential (AP) firing in small dorsal root ganglion (DRG) neurons utilizing the current-clamp technique. Our findings indicate that the inhibition rates of 30 µM Flavoxate, MFCA, and 3-methylflavone on VRAC currents approximately were 78%, 46%, and 35%, with corresponding half-maximal concentration (IC₅₀) values of 1.8 µM, 18.5 µM, and 37.2 µM, respectively. In contrast, the inhibition rates of these compounds on TMEM16A/CaCC currents approximately were 14%, 15%, and 24%, with IC₅₀ values of 32.8 µM, 28.3 µM, and 26.5 µM, respectively. These results suggest that Flavoxate is highly efficient and selective for VRAC inhibition, with the 8-substituent on its flavonoid core being crucial for this selectivity. All three flavonoids strongly inhibit AP firing, indicating that their core structure contributes to analgesic effects. In summary, Flavoxate is a selective VRAC inhibitor and a potential neuropathic pain inhibitor by suppressing AP firing in small DRG neurons.

Interstitial cells of Cajal (ICCs) are pacemaker cells that exhibit periodic spontaneous depolarization in the gastrointestinal (GI) tract and generate pacemaker potentials. In this study, we investigated the effects of ghrelin and motilin on the pacemaker potentials of ICCs isolated from the mouse small intestine. Using the whole-cell patch-clamp configuration, we demonstrated that ghrelin depolarized pacemaker potentials of cultured ICCs in a dose-dependent manner. The ghrelin receptor antagonist [D-Lys] GHRP-6 completely inhibited this ghrelin-induced depolarization. Intracellular guanosine 5'-diphosphate-${\beta}$-S and pre-treatment with $Ca^{2+}$-free solution or thapsigargin also blocked the ghrelin-induced depolarization. To investigate the involvement of inositol triphosphate ($IP_3$), Rho kinase, and protein kinase C (PKC) in ghrelin-mediated pacemaker potential depolarization of ICCs, we used the $IP_3$ receptor inhibitors 2-aminoethoxydiphenyl borate and xestospongin C, the Rho kinase inhibitor Y-27632, and the PKC inhibitors staurosporine, Go6976, and rottlerin. All inhibitors except rottlerin blocked the ghrelin-induced pacemaker potential depolarization of ICCs. In addition, motilin depolarized the pacemaker potentials of ICCs in a similar dose-dependent manner as ghrelin, and this was also completely inhibited by [D-Lys] GHRP-6. These results suggest that ghrelin induced the pacemaker potential depolarization through the ghrelin receptor in a G protein-, $IP_3$-, Rho kinase-, and PKC-dependent manner via intracellular and extracellular $Ca^{2+}$ regulation. In addition, motilin was able to depolarize the pacemaker potentials of ICCs through the ghrelin receptor. Therefore, ghrelin and its receptor may modulate GI motility by acting on ICCs in the murine small intestine.

It is known that ultrasound affects action potentials in neurons, but the underlying principles of ultrasonic neural stimulation are not clearly elucidated yet. In this study, we measured the action potentials of rat hippocampal neurons cultured on multi-electrode arrays during ultrasound stimulation. From most of electrodes, it was observed that the ultrasound stimulation increased the frequencies of action potentials (i.e., spikes) during ultrasound stimulation.

Animal experiments have shown that the positive peaked electrically compound action potentials (ECAPs) can be recorded in round window, intracochlear, and nerve trunk by stimulating a monopolar pulse. However, positive peaked ECAPs of cochlear implant recipients have never been reported because ECAPs are recorded from intracochlear electrodes after bipolar stimulation. In our experiment, the positive peaked ECAPs were recorded from 18 intracochlear electrodes in cochlear implant recipients with multiple cochlear anomalies. Thresholds in each channel were measured and the latency of P-, N-wave, and amplitude of P-N were analyzed. These results were identical with the electrically auditory brainstem response (EABR) on the input-output characteristics. In conclusion, the positive peaked ECAPs from the cochlear implant recipients are antidromic ECAPs recorded by perimodiolar electrodes stimulating cochlear implants with multiple anomalies. Therefore, positive peaked ECAPs can be used as useful audiological tools to evaluate the eighth nerve ending.

Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.

함께 투여되는 마약성진통제에 따라 효능제 또는 길항제(mixed agonist-antagonist)로 작용하는 buprenorphine을 사용하여 개구리 좌골신경에 존재하는 아편수용체의 성질을 검토하였다. 실험은 sucrose-gap apparatus를 사용하여 활동전압에 대한 영향을 관찰하였으며 약물의 상호작용을 검토하고자 meperidine 또는 naloxone을 사용하여 다음과 같은 결과를 얻었다. 1) Buprenorphine은 현저하게 개구리 좌골신경의 활동전압을 저하시켰다. 2) 두 개의 최고작용농도를 보였는데 저농도에서는 $10^{-8}\;M$, 또 고농도에서는 $10^{-4}\;M$에서 현저하게 작용을 나타내었다. 3) Buprenorphine은 meperidine의 활동전압 저하작용을 의의있게 억제하였다. 4) Naloxone에 의하여 Buprenorphine의 저하 작용이 억제되었다. 위의 실험결과로 Buprenorphine은 순수 마약성진통제의 작용을 억제하여 차단제로 작용하는 한편 또한 효능제로 활동전압을 의의있게 억제하였다. 이로써 개구리 좌골신경에 있는 아편수용체는 세포막에 또는 세포막 주위에서 $Na^+-Channel$이 활성화되는 데 중요한 역할을 하는 것으로 간주되며 이 수용체는 또한 Naloxone에 매우 민감한 반응을 나타낸다.

Buprenorphine, one of the mixed agonist-antagonist opioid drugs was used to inverstigate the opioid receptor on frog sciatic nerve A fibers. Action potentials were recorded for 4 hrs by a sucrose gap apparatus which were separated by four rubber membranes. To examine the one of the mechanism of action of buprenorphine, meperidine or naloxone was added after or before the treatment of buprenorphine. The results of this experiment were as follows: 1. Buprenorphine suppressed significantly the compound action potentials of frog sciatic nerve, and the maximal effects were shown both at $10^{-4}\;M$ and at $10^{-8}\;M$. 2. The dose-response relationship of buprenorphine on the depressant effect in frog sciatic nerve was biphasic and inverted U-shaped. 3. Buprenorphine blocked the effect of Meperidine $(10^{-3}\;M)$ on this preparation. 4. The depressant effcct of Buprenorphine on frog sciatic nerve was blocked by $10^{-8}\;M$ naloxone. From the above results, buprenorphine acts as one of agoinist-antagonistic effect on frog sciatic nerve, and the opioid receptor on this preparation is located on or near the intracellular opening of the sodium channels, which are sensitive to naloxone.

The influences of extracellular $Ca^{2+}\;and\;K^+$ upon the spike action potentials were studied in isolated uterine strips of rat. Regular, rhythmic uterine contractions were induced by the administration of oxytocin$(0.2{\sim}0.5\;I.U.)$, and recorded with force transducer. Spike action potentials were extracellularly measured by use of suction electrode, and compared with those recorded intracellularly by glass microelectrode. The results obtained were as follows : 1) The frequency and duration of spike bursts, and the number of spikes in a burst could be analyzed by use of both methods. But the absolute values of membrane potential were not measurable with the suction electrode. 2) The duration of contraction$(CD_{90};\;the\;duration\;of\;90%\;relaxation)$ was lengthened from the control 17.0 sec to 20.6 sec, in parallel with the increase of spike number from the control 21 to 26, as the increase in $Ca^{2+}$ concentration from 2 to 4 mM. 3) The amplitude and frequency of contractions were gradually decreased, simultaneously with the decrease in the number of spikes in a burst, when the $Ca^{2+}-antagonist$, verapamil was administered cumulatively. 4) The number of spikes was changed from the control 15 to 7, in cabs of the administration of ver)'low dose of verapamil$(10^{-6}\;g/l)$. 5) Increase in the numbers of spike bursts was well matched to the increase in frequency of contractions when extracellular $K^+$ was increased.

Effects of 1, 4-dihydropyridine compounds, such as nifedipine, nisoldipine, nitrendipine, and nimodipine which were calcium antagonists on the normal and Ca-dependent, slow channel mediated action potentials in the guinea pig's papillary muscle were investigated. The glass microelectrode was impaled into a papillary muscle cell for measurements of potential changes with the simultaneous tracing of isometric contraction. The concentration of Ca antagonists were 1 mg/l (nifedipine and nisoldipine), 2 mg/l (nitrendipine and nimodipine), which showed the maximal inhibition of isometric contraction (above 90%) and simultaneous effects on the normal action potentials and only the halves of those concentrations were sufficient to observe the effects on the calcium action potentials. The data for analysis were only chosen when the microelectrode was maintained in a cell throughout the experiments. 1, 4-Dihydropyridine compounds decreased the action potential duration but did not affect the resting membrane potential, overshoot, and upstroke velocity of the normal action potentials with the decrease in the isometric contraction. And with the decrease in the area and amplitude of isometric contraction, the area, amplitude, upstroke velocity and duration of Ca action potential was decreased. But the differences in the effects of the Ca antagonists were not observed. Therefore it is inferred that the changes in normal and Ca action potential induced by the 1, 4-dihydropyridine compounds with a common chemical structure would be caused by the slow inward Ca-current, not by a fast Na-current.