• BMB Reports
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• 제42권8호
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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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• 제28권6호
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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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• 제37권2호
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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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• 제11권1호
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• pp.1-15
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• 1994

• 한국응용과학기술학회지
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• 제36권3호
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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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• 제26권1호
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• pp.1-5
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• 2002

고려홍삼은 혈압강하효과가 있음이 잘 알려져 있다. 이에 백서장간막이 동맥의 저항혈관에서 고려홍삼 사포닌 성분의 혈관 이완기전을 규명하고자 내경이 150$\mu\textrm{m}$이하의 작은 혈관을 이요하여 여러 실험 조건에서 장력의 변화를 측정하여 다음과 같은 결과를 얻었다. 고려홍삼 사포닌 성분은 농도 의존적으로 (0.01mg/$m\ell$~1mg/$m\ell$) 혈관 평활근을 이완시켰으며 내피세포를 제거한 상태에서도 혈관의 이완효과는 지속되었다. A23187 이나 phorbol 12, 13-dibutyrate 에 의한 수축에서는 고려홍삼 사포닌에 의한 혈관의 이완효과가 나타나지 않았다. 고려홍삼 사포닌에 의한 혈관이완효과는 실험용액의 $K^{+}$ 농도를 증가시키면 감소되었으며 각종 $K^{+}$이 온통로 억제제인 tetaethylammonium, glybenclamide, 4-aminopyridine 및 BaCl$_2$를 전처치한 결과 BaCl$_2$에 의해서만 농도에 의존적으로 고려홍삼 사포닌에 의한 혈관이완작용이 억제되었다. 이상의 실험결과로부터 고려홍삼 사포닌은 장간막 동맥의 저항혈관에서 $K^{+}$의 유출을 증가시켜 혈관평활근을 이완시키며 $Ba^{2+}$에 의하여 차단되는 $K^{+}$ 이온통로가 고려홍삼 사포닌에 의한 혈관이완작용에 관여함을 알 수 있었다.

• Tuberculosis and Respiratory Diseases
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• 제44권5호
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• pp.1030-1039
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• 1997

연구배경 : IOS 혹은 FOT는 외부의 loudspeaker에서 발생하는 기류의 진동을 자발호흡에 부가시킴으로써 발생하는 압력의 변화를 분석하여 폐기능을 평가하는 방법으로, 일반적인 폐기능검사 방법들과는 달리 노력성 호기방법이 필요치 않고 자발성 상시호흡에서 검사가 가능하다는 장점이 있다. 또한 microprocessor 의 도입으로 Fourier 변환법에 의한 복잡한 신호 분석이 가능해 지면서 주파수에 따른 호흡기계의 impedance를 실측부분 (Rrs : resistance) 과 추정부분 (Xrs : reactance)의 두요소로 보다 깊이 파악할 수 있게 되었다. IOS의 임상적 이용은 소아의 폐기능검사, 역학적 연구, 소기도질환의 확인, 유발검사 등에 장점이 있다고 알려져 있다. 그러나 흡연자에서 발생하는 소기도 폐쇄 또는 조기 기도폐쇄를 확인하는데 있어서 IOS의 역할에 대한 연구 보고는 논란이 있어 왔다. 이에 본 연구에서는 흡연자에서의 조기 기도폐쇄를 측정하는 방법으로서의 IOS가 갖는 임상적 유용성을 검증해보고자 하였다. 방 법 : 종합검진센타를 방문한 남자중에서 노력성 호기성 폐활량 측정 검사상 정상 소견을 보인 356명($40.6{\pm}9.7$세)을 대상으로 IOS(Jaeger company : Version 4.1)을 시행하여 흡연자군 (234명 : $40.2{\pm}9.3$세)과 비흡연자군(122명 : $41.5{\pm}10.6$세)으로 구분하여 양군간에 두가지 검사볍 지표들에 대한 유의성을 검증하였다. 결 과 : Spirometry 지표인 FVC, FVC%pred, FEV1, FEV1%pred, FEV1/FVC, PEF, PEF%pred, FEF25~75%, FEF25~75%pred, FEF50%, FEF50%pred 등은 모두 흡연자군과 비흡연자군간에 유의한 차이가 관찰되지 않았다. IOS 지표중 total resistance(흡연자군 : 비 흡연자군=$2.58{\pm}1.71$ : $2.22{\pm}1.20$), peripheral resistance($1.47{\pm}0.10$ : $1.25{\pm}0.62$), bronchial compliance($0.47{\pm}0.16$ : $0.44{\pm}0.12$) 등은 양군간에 유의한(p<0.05) 차이가 관찰되었으나 central resistance와 lung compliance는 유의한 차이가 관찰되지 않았다(단위는 resistance=hPa/l/s ; compliance=1/hPa). 주파수에 따른(5, 10, 15, 20, 25, 30, 35Hz) Rrs은 양군간에 유의한 차이를 관찰할 수 없었고, Xrs는 낮은 주파수, 즉 X5($-0.76{\pm}0.48$ : $-0.62{\pm}0.28$) 와X10($-0.15{\pm}0.33$ : $-0.06{\pm}0.19$)에서 유의한 차이를 관찰할 수 있었다(단위는 hPa/l/s). 결론 : IOS은 흉연자와 비흡연자의 조기폐쇄를 확인할 수 있는 검사법이라고 판단되며, total resistance, peripheral resistance, bronchial compliance, 그리고 5Hz와 10Hz 의 낮은 주파수에서의 Xrs가 유용한 지표라고 판단된다.

• Archives of Pharmacal Research
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• 제27권4호
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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.

• 한국생명과학회:학술대회논문집
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• 한국생명과학회 2001년도 10주년 기념 국제학술 심포지움 및 추계학술대회
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• pp.35-35
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• 2001

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1998년도 춘계학술대회
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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.