WordNet
- being long-lasting and recurrent or characterized by long suffering; "chronic indigestion"; "a chronic shortage of funds"; "a chronic invalid"
- of long duration; "chronic money problems" (同)continuing
- habitual; "a chronic smoker" (同)inveterate
PrepTutorEJDIC
- (病気が)長期にわたる,慢性の / 《名詞の前にのみ用いて》常習の,癖になった
- 妨害する,じゃまする;(…を)妨害する《+『of』+『名』》
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English Journal
- The kinin B1 receptor regulates muscle-specific E3 ligases expression and is involved in skeletal muscle mass control.
- Parreiras-E-Silva LT1, Reis RI1, Santos GA1, Pires-Oliveira M2, Pesquero JB3, Gomes MD1, Godinho RO2, Costa-Neto CM.Author information 1*Department of Biochemistry and Immunology, Faculty of Medicine at Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.2†Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo, 04039-032 São Paulo, SP, Brazil.3‡Department of Biophysics, Escola Paulista de Medicina, Universidade Federal de São Paulo, 04039-032 São Paulo, SP, Brazil.AbstractRegulation of muscle mass depends on the balance between synthesis and degradation of proteins, which is under the control of different signalling pathways regulated by hormonal, neural and nutritional stimuli. Such stimuli are altered in several pathologies, including COPD (chronic obstructive pulmonary disease), diabetes, AIDS and cancer (cachexia), as well as in some conditions such as immobilization and aging (sarcopenia), leading to muscle atrophy, which represents a significant contribution to patient morbidity. The KKS (kallikrein-kinin system) is composed of the enzymes kallikreins, which generate active peptides called kinins that activate two G-protein-coupled receptors, namely B1 and B2, which are expressed in a variety of tissues. The local modulation of the KKS may account for its participation in different diseases, such as those of the cardiovascular, renal and central nervous systems, cancer and many inflammatory processes, including pain. Owing to such pleiotropic actions of the KKS by local modulatory events and the probable fine-tuning of associated signalling cascades involved in skeletal muscle catabolic disorders [for example, NF-κB (nuclear factor κB) and PI3K (phosphoinositide 3-kinase)/Akt pathways], we hypothesized that KKS might contribute to the modulation of intracellular responses in atrophying skeletal muscle. Our results show that kinin B1 receptor activation induced a decrease in the diameter of C2C12 myotubes, activation of NF-κB, a decrease in Akt phosphorylation levels, and an increase in the mRNA levels of the ubiquitin E3 ligases atrogin-1 and MuRF-1 (muscle RING-finger protein-1). In vivo, we observed an increase in kinin B1 receptor mRNA levels in an androgen-sensitive model of muscle atrophy. In the same model, inhibition of the kinin B1 receptor with a selective antagonist resulted in an impairment of atrogin-1 and MuRF-1 expression and IκB (inhibitor of NF-κB) phosphorylation. Moreover, knockout of the kinin B1 receptor in mice led to an impairment in MuRF-1 mRNA expression after induction of LA (levator ani) muscle atrophy. In conclusion, using pharmacological and gene-ablation tools, we have obtained evidence that the kinin B1 receptor plays a significant role in the regulation of skeletal muscle proteolysis in the LA muscle atrophy model.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Aug 1;127(3):185-94. doi: 10.1042/CS20130358.
- Regulation of muscle mass depends on the balance between synthesis and degradation of proteins, which is under the control of different signalling pathways regulated by hormonal, neural and nutritional stimuli. Such stimuli are altered in several pathologies, including COPD (chronic obstructive pulm
- PMID 24498923
- A murine model of airway fibrosis induced by repeated naphthalene exposure.
- Aoshiba K1, Tsuji T2, Itoh M2, Semba S2, Yamaguchi K3, Nakamura H2, Watanabe H2.Author information 1Department of Respiratory Medicine, Tokyo Medical University Ibaraki Medical Center, Japan. Electronic address: kaoshiba@tokyo-med.ac.jp.2Department of Respiratory Medicine, Tokyo Medical University Ibaraki Medical Center, Japan.3Comprehensive and Internal Medicine, Tokyo Women's Medical University Medical Center East, Japan.AbstractThe airway epithelium serves as a biological barrier essential for host defense against inhaled pollutants. While chronic epithelial injury, commonly associated with chronic obstructive pulmonary disease and bronchiolitis obliterans syndrome, often results in airway fibrosis, limited animal models of airway fibrosis have been established. Club cells (Clara cells) in the small airways represent an important population of epithelial progenitor cells and also the principal site of localization of the cytochrome P-450 monooxygenase system, which metabolically activates xenobiotic chemicals such as naphthalene by converting them to toxic epoxide intermediates. We hypothesized that repeated exposure to naphthalene may cause prolonged loss of club cells, triggering aberrant local epithelial repair mechanisms that lead to peribronchial fibrosis. We administered intraperitoneal injections of naphthalene to C57/BL6J mice once a week for 14 consecutive weeks. Repeated club cell injury caused by naphthalene triggered regional hyperproliferation of epithelial progenitor cells, while other regions remained denuded or squamated, resulting in fibroblast proliferation and peribronchial collagen deposition associated with upregulation of the fibrogenic cytokines transforming growth factor-β and connective tissue growth factor. The total collagen content of the lung assessed by measurement of the hydroxyproline content was also increased after repeated exposure to naphthalene. These results lend support to the relevance of repeated injury of airway epithelial cells as a trigger for resting fibroblast proliferation and airway fibrosis. This model of airway fibrosis is simple and easy to reproduce, and may be expected to advance our understanding of the pathogenesis and potential treatment of airway fibrotic disorders.
- Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie.Exp Toxicol Pathol.2014 Jul;66(4):169-77. doi: 10.1016/j.etp.2014.01.001. Epub 2014 Jan 28.
- The airway epithelium serves as a biological barrier essential for host defense against inhaled pollutants. While chronic epithelial injury, commonly associated with chronic obstructive pulmonary disease and bronchiolitis obliterans syndrome, often results in airway fibrosis, limited animal models o
- PMID 24480153
- Targeting the mevalonate cascade as a new therapeutic approach in heart disease, cancer and pulmonary disease.
- Yeganeh B1, Wiechec E2, Ande SR3, Sharma P4, Moghadam AR5, Post M1, Freed DH6, Hashemi M7, Shojaei S8, Zeki AA9, Ghavami S10.Author information 1Hospital for Sick Children Research Institute, Department of Physiology & Experimental Medicine, University of Toronto, Toronto, Canada.2Dept. Clinical & Experimental Medicine, Division of Cell Biology & Integrative Regenerative Med. Center (IGEN), Linköping University, Sweden.3Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.4Department of Physiology & Pharmacology, Snyder Institute for Chronic Diseases, Faculty of Medicine, University of Calgary, 4C46 HRIC, 3280 Hospital Drive NW, Calgary, Alberta, Canada.5Scientific Association of Veterinary Medicine, Faculty of Veterinary Medicine, Tabriz Branch, Islamic Azad University, Tabriz, Iran; Young Researchers and Elite Club, Ardabil Branch, Islamic Azad University, Ardabil, Iran.6Department of Physiology, St. Boniface Research Centre, University of Manitoba, Winnipeg, Canada.7Cellular and Molecular Research Center, Zahedan University of Medical Sciences, Zahedan, Iran.8Department of Biochemistry, Recombinant Protein Laboratory, Medical School, Shiraz University of Medical Sciences, Shiraz, Iran.9U.C. Davis, School of Medicine, U.C. Davis Medical Center, Department of Internal Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, Center for Comparative Respiratory Biology & Medicine, Davis, CA, USA. Electronic address: amir.zeki@ucdmc.ucdavis.edu.10Department of Human Anatomy and Cell Science, St. Boniface Research Centre, Manitoba Institute of Child Health, Biology of Breathing Theme, University of Manitoba, Winnipeg, Canada. Electronic address: ghavami@cc.umanitoba.ca.AbstractThe cholesterol biosynthesis pathway, also known as the mevalonate (MVA) pathway, is an essential cellular pathway that is involved in diverse cell functions. The enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGCR) is the rate-limiting step in cholesterol biosynthesis and catalyzes the conversion of HMG-CoA to MVA. Given its role in cholesterol and isoprenoid biosynthesis, the regulation of HMGCR has been intensely investigated. Because all cells require a steady supply of MVA, both the sterol (i.e. cholesterol) and non-sterol (i.e. isoprenoid) products of MVA metabolism exert coordinated feedback regulation on HMGCR through different mechanisms. The proper functioning of HMGCR as the proximal enzyme in the MVA pathway is essential under both normal physiologic conditions and in many diseases given its role in cell cycle pathways and cell proliferation, cholesterol biosynthesis and metabolism, cell cytoskeletal dynamics and stability, cell membrane structure and fluidity, mitochondrial function, proliferation, and cell fate. The blockbuster statin drugs ('statins') directly bind to and inhibit HMGCR, and their use for the past thirty years has revolutionized the treatment of hypercholesterolemia and cardiovascular diseases, in particular coronary heart disease. Initially thought to exert their effects through cholesterol reduction, recent evidence indicates that statins also have pleiotropic immunomodulatory properties independent of cholesterol lowering. In this review we will focus on the therapeutic applications and mechanisms involved in the MVA cascade including Rho GTPase and Rho kinase (ROCK) signaling, statin inhibition of HMGCR, geranylgeranyltransferase (GGTase) inhibition, and farnesyltransferase (FTase) inhibition in cardiovascular disease, pulmonary diseases (e.g. asthma and chronic obstructive pulmonary disease (COPD)), and cancer.
- Pharmacology & therapeutics.Pharmacol Ther.2014 Jul;143(1):87-110. doi: 10.1016/j.pharmthera.2014.02.007. Epub 2014 Feb 26.
- The cholesterol biosynthesis pathway, also known as the mevalonate (MVA) pathway, is an essential cellular pathway that is involved in diverse cell functions. The enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGCR) is the rate-limiting step in cholesterol biosynthesis and cataly
- PMID 24582968
Japanese Journal
- Comparison of Distance of 6-min Walk Test and the Incremental Shuttle Walk Test with Lung Function or Quality of Life in Patients with Chronic Obstructive Pulmonary Disease
- Ushiki Atsuhito,Fujimoto Keisaku,Ito Michiko,Yasuo Masanori,Urushihata Kazuhisa,Hanaoka Masayuki,Kubo Keishi
- 信州医学雑誌 61(2), 57-64, 2013-04-10
- NAID 120005248179
- 慢性閉塞性肺疾患(COPD)における呼吸練習のエビデンス
- Effects of Nasal Continuous Positive Airway Pressure on the Glomerular Filtration Rate in Patients with Obstructive Sleep Apnea Syndrome
- Koga Seiji,Ikeda Satoshi,Yasunaga Tomohiko,Nakata Tomoo,Maemura Koji
- Internal Medicine 52(3), 345-349, 2013-02-01
- … Objective Previous studies have shown a possible role for obstructive sleep apnea syndrome (OSAS) in the development and/or progression of chronic kidney disease (CKD). …
- NAID 120005230762
Related Links
- Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung disease (COLD), and chronic obstructive airway disease (COAD), among others, is a type of obstructive lung disease characterized by ...
- What is Chronic Obstructive Pulmonary Disease? Chronic Obstructive Pulmonary Disease is a slowly progressive serious disease of the airways that is characterized by a ...
Related Pictures
★リンクテーブル★
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慢性閉塞性気道疾患
- 関
- chronic airflow obstruction、chronic obstructive lung disease、chronic obstructive pulmonary disease、COAD、COPD
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慢性閉塞性気道疾患 COAD
[★]
慢性閉塞性肺疾患 COPD
[★]
- 関
- constrictive、obliterans、obliterative、occlusive、occlusively
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- 関
- chronically、chronicity