• Investigative Magnetic Resonance Imaging
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• v.8 no.2
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• pp.94-99
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• 2004

Purpose : To investigate the signal enhancement ratio by NOE effect on in vivo $^{31}P$ MRS in human heart muscle and liver. we also evaluated the enhancement ratios of different phosphorus metabolites, which are important in 31P MRS for each organ. Materials and Methods : Ten normal subjects (M:F = 8:2, age range = 24-32 yrs) were included for in vivo $^{31}P$ MRS measurements on a 1.5 T whole-body MRI/MRS system using $^1H-^{31}P$ dual tuned surface coil. Two-dimensional Chemical Shift Imaging (2D CSI) pulse sequence for $^{31}P$ MRS was employed in all $^{31}P$ MRS measurements. First, $^{31}P$ MRS performed without NOE effect and then the same 2D CSI data acquisitions were repeated with NOE effect. After postprocessing the MRS raw data in the time domain, the signal enhancements in percent were estimated from the major metabolites. Results : The calculated NOE enhancement for liver $^{31}P$ MRS were $\alpha-ATP\;(7\%),\;\beta-ATP\;(9\%),\;\gamma-ATP\;(17\%),\;Pi\;(1\%),\;PDE\;(19\%)$ and $PME\;(31\%)$. Because there is no creatine kinase activity in liver, PCr signal is absent. For cardiac $^{31}P$ MRS, whole body coil gave better scout images and thus better localization than surface coil. In $^{31}P$cardiac multi-voxel spectra, DPG signal increased from left to right according to the amount of blood included. The calculated enhancement for cardiac $^{31}P$ MRS were : $\alpha-ATP\;(12\%),\;\beta-ATP\;(19\%),\;\gamma-ATP\;(30\%),\;PCr\;(34\%),\;Pi\;(20\%),\;(PDE)\;(51\%),\;and\;DPG\;(72\%)$. Conclusion : Our results revealed that the NOE effect was more pronounced in heart muscle than in liver with different coupling to 1H spin system and thus different heteronuclear cross-relaxation.

• Nutrition Research and Practice
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• v.14 no.6
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• pp.606-620
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• 2020

BACKGROUND/OBJECTIVES: Although some juices affect subjective sleep quality, there is a lack of information on the effect of a specific juice on objective sleep quality and heart rate variability (HRV) during sleep; thus the present study investigated whether a blended juice made from natural extracts influenced sleep quality and HRV during sleep in adults with disturbed sleep. SUBJECTS/METHODS: A randomized, crossover study was conducted on twenty-five adults (15/10, female/male) complaining of difficulty initiating or maintaining nighttime sleep (Pittsburgh sleep quality index [PSQI] ≥ 5). During feeding sessions (FS), subjects received sleep-inducing juice made of natural ingredients (250 mL/trial) twice a day for 8 weeks or non-FS (N-FS) for 8 weeks while maintaining normal activities. Sleep quality and parameters were recorded via wearable actigraph for 7 consecutive days, and PSQI scores were assessed before and after the intervention. HRV was also monitored at rest and during sleep. RESULTS: After receiving the sleep-inducing juice intervention (FS), PSQI scores were significantly decreased (P < 0.001) and correlated with a significant decline in fatigue severity scale and visual analogue scale levels (P < 0.05; both). HRV indices of vagal activity were significantly improved during FS (P < 0.05), and no significant differences in N-FS were observed. Sleep efficiency and total sleep time increased significantly (P < 0.05) and sleep latency, total counts, sleep fragmentation index, and movement index, decreased significantly (P < 0.05, all 4) during FS, with no significant differences-observed during N-FS. CONCLUSIONS: This study results demonstrated that an 8-week course of sleep-inducing juice has led to improve sleep quality, suggesting an enhanced cardiac vagal tone during sleep. Thus, it could be a well-tolerated option for adults with disturbed sleep.

• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.113-120
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• 1990

Influences of trigger calcium on myocardial contraction from several sources were investigated on the frequency reduction-induced changes of contraction in rat left atria driven by electrical field stimulation. Rat atria elicited characteristic three phase-changes according to frequency reduction: the first rapid rise in twitch tension, the second transient fast decrease in tension and the third maintenance of twitch tension at about 200% of resting tension during high frequency. Caffeine treatment enormously suppressed the frequency reduction-induced twitch tension increase. The atrial contraction during high frequency vanished after verapamil treatment. But, during low frequency, atrial contraction revived in the presence of verapamil. Ouabain treatment and sodium depletion in superfusing solution abolished the characteristic second phase with slow frequency. These results suggest that slow calcium channel is an indispensable calcium entry route and calcium release from sarcoplasmic reticulum is an major source for trigger calcium in cardiac contraction. And sodium-calcium exchange has a modulatory roles in the regualtion of trigger calcium according to the changes of intracellular sodium concentration.

• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.121-126
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• 1990

The contractility of isolated rat atria, suspended in Krebs-Ringer bicarbonate medium containing 5.5mM glucose, was depressed approximately 50% by 0.1 mM of lidocaine. Partial recovery of the lidocaine-depressed contractility was achieved by the metabolizable substrates pyruvate, acetate, and fructose, but not by addition of glucose. Glucose produced the dose-dependent increase in the force of contraction of normal atria, whereas pyruvate, acetate, and fructose produced no significant effect in the contractile activity of the normal atria. In the absence of exogenous glucose lidocaine produced more marked depression of atrial contractility than that in the presence of exogenous glucose. The results of this study may confirm that the utilization of cardiac glycogen is also inhibited by lidocaine at sites of the glucose phosphate isomerase step or step between glycogen to glucose-6-phosphate.

• The Journal of Korean Institute of Electromagnetic Engineering and Science
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• v.27 no.3
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• pp.299-306
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• 2016

In this paper, a vital sign sensor based on impedance variation of resonator is proposed to detect the respiration and heartbeat signals within near-field range as a function of the separation distance between resonator and subject. The sensor consists of an oscillator with a built-in planar type patch resonator, a diplexer for only pass the second harmonic frequency, amplifier, SAW filter, and RF detector. The cardiac activity of a subject such as respiration and heartbeat causes the variation of the oscillation frequency corresponding impedance variation of the resonator within near-field range. The combination of the second harmonic oscillation frequency deviation and the superior skirt frequency of the SAW filter enables the proposed sensor to extend twice detection range. The experimental results reveal that the proposed sensor placed 40 mm away from a subject can reliably detect respiration and heartbeat signals.

• Toxicological Research
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• v.11 no.1
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• pp.161-168
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• 1995

It has been found that various stress challenges induce the myocardial antioxidant enzymes and produce an acquisition of the cellular resistance to the ischemic injury in animal hearts. Most of the stresses, however, seem to be guite dangerous to an animal's life. In the present study, therefore, we tried to search for safely applicable stress modalities which could lead to the induction of antioxidant enzymes and the production of myocardial tolerance to the ischemia-reperfusion injury. Male Sprague-Dawley rats (200-250 g) were exposed to various non-fatal stress conditions, i.e., hyperthermia (environmental temperature of $42^{\circ}C$ for 30 min, non-anesthetized animal), iramobilization (60 min), treadmill exercise (20 m/min, 30min), swimming (30 min), and hyperbaric oxyflenation (3 atm, 60 min), once a day for 5 days. The activities of myocardial antioxidant enzymes and the ischemia-reperfusion injury of isolated hearts were evaluated at 24 hr after the last application of the stresses. The activities of antioxidant enzymes, superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase (G6PD), were assayed in the freshly excised ventricular tissues. The ischemia-reperfusion injury was produced by 20 min-global ischemia followed by 30 min-reperfusion using a Langendorff perfusion system. In swimming and hyperbaric oxygenation groups, the activities of SOD and G6PD increased significantly and in the hyperthermia group, the catalase activity was elevated by 63% compared to the control. The percentile recoveries of cardiac function at 30 min of the post-ischemic reperfusion were 55.4%, 73.4%, and 74.2% in swimming, the hyperbaric oxygenation and the hyperthermia groups, respectively. The values were significantly higher than that of the control (38.6%). In additions, left ventricular end-diastolic pressure and lactate dehydrogenase release were significantly reduced in the stress groups. The results suggest that the antioxidant enzymes in the heart could be induced by the apparently safe in vivo-stresses and this may be involved in the myocardial protection from the ischemia-reperfusion injury.

• The Journal of Internal Korean Medicine
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• v.26 no.4
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• pp.844-852
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• 2005

Objectives : Through spectral analysis of heart rate variability(HRV) to study autonomic nervous system dysfunction of Hwabyung, culture related disease in Korea. Methods : HRV of 18 patients diagnosed as Hwabyung was measured against 13 healthy controls. HRV was measured by SA-2000p(Mediocre, Korea) for five minutes after 5 minutes resting. Results : 1. In time domain analysis, mean pulse rate(PRT) of in Hwabyung group was significantly higher than healthy controls. Standard deviation of all normal P-P intervals(SDNN), the square root of the mean of the sum of the squares of differences between adjacent normal P-P intervals(RMS-SD) in Hwabyung group was lower than healthy controls, but not significant. 2. As for frequency domain analysis, In TP(logarithmic total power), In VLF(logarithmic very low frequency), and In LF(logarithmic low frequency )in Hwabyung group was significantly lower than healthy controls. Ln HF(logarithmic high frequency), LF/HF ratio in Hwabyung group was also lower but not significant. Conclusions : This study suggests tile activity and imbalance of cardiac autonomous nervous system in Hwabyung patient is significantly lower than healthy individuals.

• Journal of Chest Surgery
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• v.19 no.2
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• pp.225-231
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• 1986

Pericardial adhesions following open heart surgery pose a special problems, increasing the risk of cardiac reoperation because of the danger of damaging the heart, coronary artery and veins, or grafts and also the fibrous tissue may obliterate the pericardial space and eventually constrict the heart. This study was undertaken to evaluate the effect of intrapericardial urokinase and dextran 40 on the formation of pericardial adhesions in an animal model. latrogenic traumas on the pericardium were surgically induced in 30 rabbits, simulating injuries possible during actual surgery. In all rabbits, blood [1 ml] was obtained from an ear vessel and injected into the pericardium. Control group of ten rabbits did not receive any further medication, urokinase group of ten received 15, 000-20, 000 IU of urokinase, and remained ten received 1 ml of 10% dextran 40. All rabbits were sacrificed at 4 weeks. At autopsy, the development of adhesions were graded as none [Grade I], minimal [Grade II], moderate [Grade III], and severe [Grade IV]. Histological studies of the parietal pericardium and epicardium were performed. The results were as follows: 1. Group 1[Control group] showed minimal adhesion in 40%, moderate in 50%, and severe in 10% of the group. Sharp dissections were necessary in 60% of adhesions. 2. Group II [Dextran group] showed no adhesions in 20%, minimal in 60%, and moderate in 20% of the group. 3. Group III [Urokinase group] showed no adhesions in 40%, minimal in 40%, and moderate in 20% of the group. Considering in this group, the adhesion activity was significantly suppressed [60% adhesions] compared to the control group [100% adhesions] [P < 0.05]. 4. Histological findings revealed mild serosal fibrosis in none adherent group, loose fibrous connections between two layers of pericardium in minimal adhesion group, tight fibrous connections in moderate adhesion group, and marked fibrous thickening and close attachment of two surfaces were noted in severe adhesion group. These data have revealed the decreased incidence of pericardial adhesions with urokinase and dextran 40.

• Journal of Chest Surgery
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• v.18 no.1
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• pp.97-103
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• 1985

During the period of seven years from Jan. 1976 to Jan. 1983, one hundred cases of pulmonary tuberculous residual lesions were resected at the Department of Thoracic Surgery, Paik Hospital in Seoul, Korea. During the period of this study, 1764 patients were admitted with the diagnosis of pulmonary and/or pleural tuberculosis in the medical and surgical department as a primary or associated conditions. Among these 1764 patients, one hundred selective cases were operated. The results were as follows; l. Extents of the disease by the predominant clinical pictures were: totally destroyed lung; 18, destroyed lobe; 6, cavitary lesion with or without positive sputum; 35, bronchiectasis; 7, bronchostenosis with atelectasis; 2, empyema with or without BPF; 20, pleural thickening; 4, tuberculoma; 3, bullous cyst with tuberculosis; 5 cases, or per cent [Table 1]. 2. Male and female ratio was 1.2:1 or 55 and 45 per cent. Age distribution ranged 15 and 55 with average of 33 years [Table 2]. 3. Type of procedures were: pleuropneumonectomy; 15, pneumonectomy; 25, lobectomy; 37, bilobectomy; 6, lobectomy plus segmentectomy; 3, pleurectomy; 14 cases, or percent, Site of resections were: right; 58 and left; 42 cases, or per cent [Table 3]. 4. Incidence of complications were 10 per cent and the mortality was 4 per cent. The causes of morbidity were analyzed. The main causes of death were pulmonary insufficiency; 2, cardiac arrhythmia; 1, and hepatic insufficiency; 1 case or per cent [Table 4]. 5. Pathologic examinations of the resected pulmonary and pleuropulmonary lesions were observed by gross specimen, correlating with the pre-operative indications of the disease [Fig. 1, 2, 3, 4, 5, 6].>br> 6. Anti-tuberculous chemotherapy was done for 6 to 18 months, post-operatively, in 80 patients. Of these 49 cases were need medication for 12 months [Table 5]. Except the four operative mortality and a case of post-operative recurrent buberculosis under medication, all the other 95 cases are well in activity and free from the disease at the moment.

• Toxicological Research
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• v.34 no.2
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• pp.143-150
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• 2018

It has been demonstrated that vanadate causes nephrotoxicity. Vanadate inhibits renal sodium potassium adenosine triphosphatase (Na, K-ATPase) activity and this is more pronounced in injured renal tissues. Cardiac cyclic adenosine monophosphate (cAMP) is enhanced by vanadate, while increased cAMP suppresses Na, K-ATPase action in renal tubular cells. There are no in vivo data collectively demonstrating the effect of vanadate on renal cAMP levels; on the abundance of the alpha 1 isoform (${\alpha}_1$) of the Na, K-ATPase protein or its cellular localization; or on renal tissue injury. In this study, rats received a normal saline solution or vanadate (5 mg/kg BW) by intraperitoneal injection for 10 days. Levels of vanadium, cAMP, and malondialdehyde (MDA), a marker of lipid peroxidation were measured in renal tissues. Protein abundance and the localization of renal ${\alpha}_1-Na$, K-ATPase was determined by Western blot and immunohistochemistry, respectively. Renal tissue injury was examined by histological evaluation and renal function was assessed by blood biochemical parameters. Rats treated with vanadate had markedly increased vanadium levels in their plasma, urine, and renal tissues. Vanadate significantly induced renal cAMP and MDA accumulation, whereas the protein level of ${\alpha}_1-Na$, K-ATPase was suppressed. Vanadate caused renal damage, azotemia, hypokalemia, and hypophosphatemia. Fractional excretions of all studied electrolytes were increased with vanadate administration. These in vivo findings demonstrate that vanadate might suppress renal ${\alpha}_1-Na$, K-ATPase protein functionally by enhancing cAMP and structurally by augmenting lipid peroxidation.