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Lee Soo Jin,Oh Da Yoon,Park Jae Eun,Lee Min Cheol,Jeon Myung Kyu,Jang Yeong Suk,Kim Hyeon Jin,Ahn Jae Young,Hong Noo ri,Kim Woo Young 대한침구의학회 2020 대한침구의학회지 Vol.37 No.2
The purpose of this review was to evaluate the effectiveness of electroacupuncture treatment for women with “primary obesity.” Primary obesity is caused by an imbalance in energy intake and consumption due to abnormal eating and living habits in the absence of specific diseases causing the obesity. A literature review (up to December 2019) of randomized controlled trials (RCT) of electroacupuncture treatment for women with “primary obesity” was performed. Relevant clinical studies were retrieved from several databases, and interventions and results were analyzed. There were 6 RCT that fitted the inclusion criteria for this review. The intervention for the treatment group of the selected 6 RCT was electrical stimulation applied to acupoints. Interventions for the control groups included non-treatment, general acupuncture, and so on. Indicators for assessing treatment effects varied from study to study. Four out of 5 studies used body mass index (BMI) as an assessment tool and showed a significant decrease in BMI following electroacupuncture treatment. There were 4 studies using waist circumference as an indicator of abdominal obesity and these studies showed a significant decrease in waist circumference following electroacupuncture treatment. Electroacupuncture treatment used in primary obese women had a clinically significant effect, however, further RCT are needed.
Lee, Youn-Ri,Lee, Chang-Kwon,Park, Hyo-Jun,Kim, Hyo-Jin,Kim, Jung-Hwan,Kim, Jae-Heung,Lee, Keun-Sang,Lee, Yun-Lyul,Min, Kyung-Ok,Kim, Bo-Kyung Korean Physical Therapy Science 2006 대한물리치료과학회지 Vol.13 No.2
Vascular smooth muscle contraction is mediated by activation of extracellular signal-regulated kinase (ERK) 1/2, an isoform of mitogen-activated protein kinase (MAPK). However, the role of stress-activated protein kinase/c-Jun N-terminal kinase (JNK) in vascular smooth muscle contraction has not been defined. We investigated the role of JNK in the contractile response to norepinephrine (NE) in rat aortic smooth muscle. NE evoked contraction in a dose-dependent manner, and this effect was inhibited by the JNK inhibitor SP600125. NE increased the phosphorylation of JNK, which was greater in aortic smooth muscle from hypertensive rats than from normotensive rats. NE-induced JNK phosphorylation was significantly inhibited by SP600125 and the conventional-type PKC (cPKC) inhibitor Go6976, but not by the Rho kinase inhibitor Y27632 or the phosphatidylinositol 3-kinase inhibitor LY294002. Thymeleatoxin, a selective activator of cPKC, increased JNK phosphorylation, which was inhibited by $G{\ddot{o}}6976$. SP600125 attenuated the phosphorylation of caldesmon, an actin-binding protein whose phosphorylation is increased by NE. These results show that JNK contributes to NE-mediated contraction through phosphorylation of caldesmon in rat aortic smooth muscle, and that this effect is regulated by the PKC pathway, especially cPKC.
Antioxidant Down-Regulates Interleukin-18 Expression in Asthma
Lee, Kyung Sun,Kim, So Ri,Park, Seoung Ju,Min, Kyung Hoon,Lee, Ka Young,Jin, Sun Mi,Yoo, Wan Hee,Lee, Yong Chul American Society for PharmacologyExperimental Ther 2006 Molecular pharmacology Vol.70 No.4
<P>An alteration in the balance between a T-helper type 2 cell (Th2) response and a Th1 response may predispose to the development of bronchial asthma. Interleukin-18 (IL-18) has an ability to promote both Th1 and Th2 responses, depending on the surrounding cytokine environment. Reactive oxygen species (ROS) play a crucial role in the pathogenesis of airway inflammation and hyperresponsiveness. Recent studies have demonstrated that antioxidants are able to reduce airway inflammation and hyperreactivity in animal models of asthma. In this study, we used a C57BL/6 mouse model of allergic asthma to examine the effects of antioxidants on the regulation of IL-18 expression. Our present study with ovalbumin-induced murine model of asthma revealed that ROS production in cells from bronchoalveolar lavage fluids was increased and that administration of L-2-oxothiazolidine-4-carboxylic acid or alpha-lipoic acid reduced the increased levels of ROS, the increased expression of IL-18 protein and mRNA, airway inflammation, and bronchial hyperresponsiveness. Our results also showed that antioxidants down-regulated a transcription factor, nuclear factor-kappaB (NF-kappaB), activity. These results indicate that antioxidants may reduce IL-18 expression in asthma by inhibiting the activity of NF-kappaB and suggest that ROS regulate the IL-18 expression.</P>
Lee, Kyung Sun,Kim, So Ri,Park, Seoung Ju,Lee, Ho Kyung,Park, Hee Sun,Min, Kyung Hoon,Jin, Sun Mi,Lee, Yong Chul American Society for PharmacologyExperimental Ther 2006 Molecular pharmacology Vol.69 No.6
<P>Vascular endothelial growth factor (VEGF) plays a pivotal role in the pathogenesis of bronchial asthma. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) has been implicated in regulating cell survival signaling through the phosphoinositide 3-kinase (PI3K)/Akt pathway. The key role of PI3K in VEGF-mediated signal transduction is established. However, the effects of PTEN on VEGF-mediated signaling in asthma are unknown. This study aimed to determine the effect of PI3K inhibitors and PTEN on VEGF expression in allergen-induced airway inflammation. We have used a female C57BL/6 mouse model for asthma to determine the role of PTEN in allergen-induced airway inflammation, specifically in the expression of VEGF. Allergen-induced airway inflammation leads to increased activity of PI3K in lung tissue. These mice develop the following typical pathophysiological features of asthma in the lungs: increased numbers of inflammatory cells of the airways; airway hyper-responsiveness; increased expression of interleukin (IL)-4, IL-5, IL-13, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, regulated on activation normal T cell expressed and secreted (RANTES), and eotaxin; increased vascular permeability; and increased levels of VEGF. Administration of PI3K inhibitors or adenoviruses carrying PTEN cDNA reduced the symptoms of asthma and decreased the increased levels of plasma extravasation and VEGF in allergen-induced asthmatic lungs. These results indicate that PTEN reduces VEGF expression in allergen-induced airway inflammation.</P>
Lee, Ji-Eun,Jin, Yong-ri,Seo, Joo-beom,Yoon, Il,Song, Mi-Ryoung,Lee, So-Young,Park, Ki-Min,Lee, Shim-Sung Korean Chemical Society 2006 Bulletin of the Korean Chemical Society Vol.27 No.2
Isomeric series of dilinked $NO_2S_2$ macrocycles ($L^2$: para-, $L^3$: meta- and $L^4$: ortho-linked) capable of binuclear complexing ability were prepared from its monomeric analog $L^1$ in reasonable yields except ortho-type reaction, which led to mixture due to the formation of monomer-type macrocyclic quaternary ammonium bromide $L^5$. Moreover, L2 (as $2HNO_3$ form) and $L^5$ were confirmed by an X-ray crystallography. Reaction of $HgCl_2$ with $L^2$ yielded a binuclear complex $[Hg_2(L^2)Cl_4]$. In the complex, each mercury(II) has a distorted tetrahedral environment made up of S and N donors from an exodentate $L^2$ and two coordinated Cl atoms.