• Journal of Chest Surgery
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• v.32 no.5
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• pp.422-427
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• 1999

Background: Tachycardia induced heart failure model would be the model of choice for the dilated cardiomyopathy. This more closely resembles the clinical syndrome and does not require major surgical trauma, myocardial ischemia and pharmacological or toxic depression of cardiac function. When heart failure is progressive, application of new surgical procedures to the faling heart is highly risky. It has been shown that recovery trajectory from heart failure is a new method in decreasing animal mortality. The purpose is to establish the control datas for recovery trajectory in the canine heart failure model. Material and Method: 21 mongrel dogs were studied at 4 stages(baseline, at the heart failure, 4 and 8 weeks after recovery). Heart failure was induced during 4 weeks of continuous rapid pacing using a pacemaker. Eight weeks of trajectory of recovery period was allowed. Indices of left ventricular function and dimension were measured every 2 weeks and the hemodynamics were measured by use of Swan-Ganz catheterization and thermodilution method every 4 weeks. Values were expressed as mean${\pm}$standard deviation. Result: 4(20%) dogs died due to heart failure. Left ventricular end-diastolic volume at the 4 stages were 40.8${\pm}$7.4, 82.1${\pm}$21.1, 59.9${\pm}$7.7 and 46.5${\pm}$6.5ml. Left ventricular end-systolic volume showed the same trend. Ejection fractions were 50.6${\pm}$4.1, 17.5${\pm}$5.8, 36.3${\pm}$7.3, and 41.5${\pm}$2.4%. Blood pressure and heart rate showed no significant changes. Pressures of central vein, right ventricle, pulmonary artery, and pulmonary capillary wedge showed significant increase during the heart failure period, normalizing at the end of recovery period. Stroke volumes were 21.5${\pm}$8.2, 12.3${\pm}$3.5, 17.9${\pm}$4.6, and 15.5${\pm}$3.4ml. Blood norepinephrine level was 133.3${\pm}$60.0pg/dL at the baseline and 479.4${\pm}$327.3pg/dL at the heart failure stage(p=0.008). Conclusion: Development of tachycardia induced heart failure model is of high priority due to ready availability and reasonable amenability to measurements. Recovery trajectory after cessation of tachycardia showed reduction of cardiac dilatation and heart function. Application of new surgical procedures during the recovery period could decrease animal mortality.

• Journal of Life Science
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• v.29 no.6
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• pp.747-753
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• 2019

Cognitive decline is characterized by reduced long-/short-term memory and attention span, and increased depression and anxiety. Such decline is associated with various degenerative brain disorders, especially Alzheimer's disease (AD) and Parkinson's disease (PD). The increases in elderly populations suffering from cognitive decline create social problems and impose economic burdens, and also pose safety threats; all of these problems have been extensively researched over the past several decades. Possible causes of cognitive decline include metabolic and hormone imbalance, infection, medication abuse, and neuronal changes associated with aging. However, no treatment for cognitive decline is available. In neurodegenerative diseases, changes in the gut microbiota and gut metabolites can alter molecular expression and neurobehavioral symptoms. Changes in the gut microbiota affect memory loss in AD via the downregulation of NMDA receptor expression and increased glutamate levels. Furthermore, the use of probiotics resulted in neurological improvement in an AD model. PD and gut microbiota dysbiosis are linked directly. This interrelationship affected the development of constipation, a secondary symptom in PD. In a PD model, the administration of probiotics prevented neuron death by increasing butyrate levels. Dysfunction of the blood-brain barrier (BBB) has been identified in AD and PD. Increased BBB permeability is also associated with gut microbiota dysbiosis, which led to the destruction of microtubules via systemic inflammation. Notably, metabolites of the gut microbiota may trigger either the development or attenuation of neurodegenerative disease. Here, we discuss the correlation between cognitive decline and the gut microbiota.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.321-330
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• 1994

The protective effect of 'ischemic preconditioning (PC)' on ischemia-reperfusion injury of heart has been reported in various animal species, but without known mechanisms in detail. In an attempt to investigate the cardioprotective mechanism of PC, we examined the effects of PC on the myocardial oxidative injuries and the oxygen free radical production in the ischemia-reperfusion model of isolated Langendorff preparations of rat hearts. PC was performed with three episodes of 5 min ischemia and 5 min reperfusion before the induction of prolonged ischemia (30 min)-reperfusion(20 min). PC prevented the depression of cardiac function (left ventricular pressure x heart rate) observed in the ischemic-reperfused heart, and reduced the release of lactate dehydrogenase during the reperfusion period. On electron microscopic pictures, myocardial ultrastructures were relatively well preserved in PC hearts as compared with non-PC ischemic-reperfused hearts. In PC hearts, lipid peroxidation of myocardial tissue as estimated from malondialdehyde production was markedly reduced. PC did not affect the activity of xanthine oxidase which is a major source of oxygen radicals in the ischemic rat hearts, but the myocardial content of hypoxanthine (a substrate for xanthine oxidase) was much lower in PC hearts. It is suggested from these results that PC brings about significant myocardial protection in ischemic-reperfused heart and this effect may be related to the suppression of oxygen free radical reactions.

• Journal of Life Science
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• v.32 no.8
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• pp.601-610
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• 2022

P. tenebrifer (PT) belongs to the Diptera order and Stratiomyidae family. Recently, insect industry have been focused as food, animal feed and environmental advantages. γ-aminobutyric acid (GABA) and melatonin have been associated with regulating sleep and depression. GABA is the primary inhibitory neurotransmitter and is synthesized via biotransformation of monosodium glutamate (MSG) to GABA by lactic acid bacteria. In this study, we first used a GABA-enhanced PT extract, wherein GABA was enhanced by feeding MSG to PT. The underlying mechanisms preventing stress and insomnia were investigated in a corticosterone (CORT)-induced endoplasmic reticulum (ER) stress and chronic restraint stress (CRS)-exposed mouse model, as well as in pentobarbital (45 mg/kg)-induced sleep behaviors in mice. In the present study, the GABA peak was detected in high-performance liquid chromatography-evaporative light scattering detector (HPLC-ELSD) analysis and showed in Ptecticus tenebrifer water extract (PTW) but not in non-PTW extract. The results showed that PTW and Ptecticus tenebrifer with 70% ethanol extract (PTE) exerted neuroprotective effects by protecting against CORT-induced downregulation of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2) and cAMP-response element binding protein (CREB) expression. In addition, PTW (300 mg/kg) significantly reduced CORT levels in CRS-exposed mice. Furthermore, PTW (100 and 300 mg/kg) significantly reduced sleep latency and increased total sleep duration in pentobarbital (45 mg/kg)-induced sleeping behaviors, which was related to serum melatonin levels. In conclusion, our results suggest that PTW exerts anti-stress and sleep-enhancing effects by regulating serum CORT and melatonin levels.