• BMB Reports
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• v.42 no.8
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• pp.475-481
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• 2009

Emerging data demonstrate pivotal roles for brain insulin resistance and insulin deficiency as mediators of cognitive impairment and neurodegeneration, particularly Alzheimer's disease (AD). Insulin and insulin-like growth factors (IGFs) regulate neuronal survival, energy metabolism, and plasticity, which are required for learning and memory. Hence, endogenous brain-specific impairments in insulin and IGF signaling account for the majority of AD-associated abnormalities. However, a second major mechanism of cognitive impairment has been linked to obesity and Type 2 diabetes (T2DM). Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death. In essence, there are dual mechanisms of brain insulin resistance leading to AD-type neurodegeneration: one mediated by endogenous, CNS factors; and the other, peripheral insulin resistance with excess cytotoxic ceramide production.

• Smart Structures and Systems
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• v.28 no.6
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• pp.737-744
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• 2021

In this study, structural health monitoring (SHM) methods of carbon fiber reinforced plastics (CFRPs) were investigated using electrical resistance. The developed sensing technique monitored electrical resistance in accordance with the impact damage of a CFRP. The changes in electrical resistances with multiple electrode sets enabled SHM without extra sensors so that this technique can be called self-sensing. Moreover, this study proposed electrodes only at peripheral side of a structure to minimize the number of electrodes compared to those in an array which has square number of sensors as the sensing area increases. For the intensive investigation, electromechanical sensitivity in terms of electrode distance was analyzed and optimized under drop weight impact testing. Then, SHM methods with electrodes in an array and electrodes in peripheral edges were comparatively investigated. The developed methods successfully localized impact damages into 2D coordinates. Furthermore, damage severity can be shown with a damage map by calculating electrical resistance change ratio. Therefore, structural health self-sensing system using electrical resistance was successfully developed with the minimum number of electrodes.

• Parasites, Hosts and Diseases
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• v.37 no.2
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• pp.101-107
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• 1999

Rats were immunized through an initial infection with 1,000 filariform larvae (L3) of Nippostrongylus brasiliensis and after complete expulsion of worms they were challenged with 1,000 L3 of Strongyloides venezuelensis to investigate whether cross-resistance developed against a heterologous parasite. Nippostrongylus brasiliensis immunized rats developed a partial cross-resistance against S.venezuelensis migrating larvae (MSL3) in the lungs and adult worms in the small intestine. The population of MSL3 in the lungs were significantly lower (p<0.05) in immunized rats($22.0{\;}{\pm}{\;}7.4$) compared with controls ($105.0{\;}{\pm}{\;}27.6$). The populations of adult worms, egg output and fecundity were initially decreased but from day 14 post-challenge they did not show any significant difference between immunized and control rats. However, the length of worm in immunized rat was revealed as retardation. Peripheral blood eosinophilia was significantly decreased (P<0.05) on day 7 post-challenge and then gradually increased which peaked on da 42 post-challenge when most of the worms were expelled. these results suggest that peripheral blood eosinophilia is strongly involved in the worm establishment and expulsion mechanisms.

• Journal of Yeungnam Medical Science
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• v.11 no.1
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• pp.1-15
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• 1994

• Journal of the Korean Applied Science and Technology
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• v.36 no.3
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• pp.876-884
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• 2019

We investigated the effect of moderate- and high-intensity resistance training on hippocampal neurotrophic factors and peripheral CCL11 levels in high-fat diet (HFD)-induced obese mice. C57/black male mice received a 4 weeks diet of normal (control, CON; n = 9) or a high-fat diet (HF; n = 27) to induce obesity. Thereafter, the HF group was subdivided equally into the HF, HF + moderate-intensity exercise (HFME), and HF + high-intensity exercise (HFHE) groups (n = 9, respectively), and mice were subjected to ladder-climbing exercise for 8 weeks. The hippocampal brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) levels were significantly lower in the HF group than in the CON group (p < 0.05). In addition, in the HFME and HFHE groups were significantly higher than in the HF group (p < 0.05). The peripheral CCL11 levels were significantly higher in the HF group than in the CON group (p < 0.05). In addition, in the HFME and HFHE groups were significantly lower than in the HF group (p < 0.05). However, there was no significant difference according to the exercise intensity among the groups. Collectively, these results suggest that obesity can induce down-regulation of neurotrophic factors and inhibition of neurogenesis. In contrast, regardless of exercise intensity, resistance training may have a positive effect on improving brain function by inducing increased expression of neurotrophic factors.

• Journal of Ginseng Research
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• v.26 no.1
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• pp.1-5
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• 2002

It has been well known that Korea red ginseng has an antihypertensive effect. The antihypertensive effect may be due to its ability to change the peripheral resistance. Change of vascular tone in the resistance-sized artery contribute to the peripheral resistance, thereby regulate the blood pressure. Therefore, we investigated to clarify the vasorelaxing mechanism induced by crude saponin of Korea red ginseng in the resistance-sized mesenteric artery of rats. The resistance-sized mesenteric artery was isolated and cut into a ring. The ring segment was immersed in HEPES-buffered solution and its isometric tension was measured using myograph force-displacement transducer. Crude saponin of ginseng relaxed the mesenmetric arterial rings precontracted with norepinephrine (3$\mu$M) in dose-dependent manner (0.01 mg/㎖ -1 mg/㎖. The relaxation by crude saponin was smaller in endothelium-intact preparation than that in endothelium-denuded preparation. The contraction induced by A23187 or phorbol 12,13-dibutyrate was not affected by crude saponin of ginseng. The vasorelaxing effect of crude saponin of ginseng was significantly attenuated by the increase of the extracellular K$\^$+/ concentration. Crude saponin-induced vasorelaxation was not affected by tetraethylammonium (1 mM), glybenclamide (10$\mu$M), and 4-aminopyridine (0.1 mM) in these preparations. Ba$\^$2+/(10$\mu$M ∼100$\mu$M) markedly reduced the crude saponin-induced vasorelakation dose-dependently. From the above results, we suggest that crude saponin of ginseng may stimulate K$\^$+/ efflux and hyperpolarize the membrane, thereby cause the vasorelaxation in the resistance-sized mesenteric artery of rats.

• Tuberculosis and Respiratory Diseases
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• v.44 no.5
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• pp.1030-1039
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• 1997

Background : Impulse Oscillometry is a noninvasive and effort-independent test used to characterize the mechanical impedance of the respiratory system. The clinical potential of the IOS is rapid and demands only passive cooperation which makes it especially appealing for children, for epidemiologic surveys and for conditions in which quiet breathig instead of forced expiratory maneuvers are preferred. However, several studies have shown conflicting results that the role of IOS about detection of smoking induced small airway diseases or early airway obstruction Methods : Study was to evaluate the clinical ability of the IOS to detect about smoking induced early airway obstruction in persons with normal spirometry test. Respiratory asymptomatic study groups were formed that one is non-smoking group, another is smoking group. Results : The parameters of spirometry were not significantly differences between non-smoking group and smoking group. Among the parameters of IOS, total resistance(non-smoking group : smoking group=$2.22{\pm}1.20$ : $2.58{\pm}1.71$), peripheral resistance($1.25{\pm}0.62$ : $1.47{\pm}0.10$), bronchial compliance($0.44{\pm}0.12$ : $0.47{\pm}0.16$) were not statistically significant different (p<0.05), but central resistance and lung compliance were not statistically significant different (unit ; resistance=hPa/l/s, compliance=l/hPa). Resistance(Rrs) was not statistically significant different with changes of frequences(5, 10, 15, 20, 25, 30, 35Hz), but Reactance(Xrs) was statistically significant different with low frequences that X5(non-smoking group : smoking group=$-0.62{\pm}0.28$ : $-0.76{\pm}0.48$, p<0.001) and X10($-0.06{\pm}0.19$ : $-0.15{\pm}0.33$, p<0.013) (unit; hPall/s, $hPa{\cong}cmH_2O$). Conclusion : Impulse oocillometer(IOS) is clinically available method to detect about smoking induced early airway obstruction. And clinically potential parameters of IOS were considers that total resistance, peripheral resistance, bronchial resistance, and reactance of low frequency at 5Hz, 10Hz.

• Archives of Pharmacal Research
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• v.27 no.4
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• pp.361-370
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• 2004

The discovery of insulin receptor substrate (IRS) proteins and their role to link cell surface receptors to the intracellular signaling cascades is a key step to understanding insulin and insulin-like growth factor (IGF) action. Moreover, IRS-proteins coordinate signals from the insulin and IGF receptor tyrosine kinases with those generated by proinflammatory cytokines and nutrients. The IRS2-branch of the insulin/IGF signaling cascade has an important role in both peripheral insulin response and pancreatic $\beta$-cell growth and function. Dysregulation of IRS2 signaling in mice causes the failure of compensatory hyperinsulinemia during peripheral insulin resistance. IRS protein signaling is down regulated by serine phosphorylation or protea-some-mediated degradation, which might be an important mechanism of insulin resistance during acute injury and infection, or chronic stress associated with aging or obesity. Under-standing the regulation and signaling by IRS1 and IRS2 in cell growth, metabolism and survival will reveal new strategies to prevent or cure diabetes and other metabolic diseases.

• Proceedings of the Korean Society of Life Science Conference
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• 2001.09a
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• pp.35-35
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• 2001

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.05a
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• pp.1-4
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• 1998

Impaired insulin action in Type 2 diabetes is thought to lead to hyperglycemia, with both environmental and complex genetic factors playing key roles. Although the primary lesion in Type 2 diabetes is unknown, a number of studies suggest that metabolic defects in the liver, skeletal muscle and fat, and pancreatic ${\beta}$-cells contribute to the disease. These metabolic abnormalities are characterized by the overproduction of hepatic glucose, impaired insulin secretion, and peripheral insulin resistance. In current pharmacological treatment of Type 2 diabetes, sulfonylurea (SU) drugs have mainly been used as oral hypoglycemic drugs to stimulate endogenous insulin secretion from ${\beta}$ cells. SU drugs, however, sometimes aggravate the disease by causing fatigue of the pancreatic ${\beta}$ cells, which leads to reduced drug efficacy after long-term treatment. This class of drugs also leads to enhanced obesity arising from the stimulation of endogenous insulin secretion in obese Type 2 diabetic patients, plus an increased incidence of SU-induced hypoglycemia. Since 1980, a major challenge has been made by us to develop a potential pharmacological therapy for the treatment of insulin resistance in peripheral tissues and/or suppression of abnormal hepatic glucose production in Type 2 diabetic patients. Such a drug would be expected to have fewer side effects and retain long-term efficacy.