WordNet

the 3rd letter of the Roman alphabet (同)c
(music) the keynote of the scale of C major
a general-purpose programing language closely associated with the UNIX operating system
tell a relatively insignificant lie; "Fibbing is not acceptable, even if you dont call it lying"
a trivial lie; "he told a fib about eating his spinach"; "how can I stop my child from telling stories?" (同)story, tale, tarradiddle, taradiddle
a slender and greatly elongated substance capable of being spun into yarn (同)fibre
a leatherlike material made by compressing layers of paper or cloth (同)fibre, vulcanized fiber
any of several elongated, threadlike cells (especially a muscle fiber or a nerve fiber) (同)fibre
a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response

PrepTutorEJDIC

carbonの化学記号
(ささいな,罪のない)うそ / 軽いうそをつく
=sense organ / 受信装置
肺の;肺を冒す

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1. 成人における肺静脈閉塞症の疫学、病因、臨床評価および診断 epidemiology pathogenesis clinical evaluation and diagnosis of pulmonary veno occlusive disease in adults
2. アミオダロンによる肺毒性 amiodarone pulmonary toxicity
3. 鎌状細胞貧血における臨床的ばらつき clinical variability in sickle cell anemia
4. 成人における過敏性腸症候群の治療 treatment of irritable bowel syndrome in adults
5. 呼吸困難の生理学 physiology of dyspnea

English Journal

Sensory Nerve Terminal Mitochondrial Dysfunction Induces Hyperexcitability in Airway Nociceptors via Protein Kinase C.

Hadley SH1, Bahia PK, Taylor-Clark TE.Author information 1University of South Florida.AbstractAirway sensory nerve excitability is a key determinant of respiratory disease-associated reflexes and sensations such as cough and dyspnea. Inflammatory signaling modulates mitochondrial function and produces reactive oxygen species (ROS). Peripheral terminals of sensory nerves are densely packed with mitochondria, thus we hypothesized that mitochondrial modulation would alter neuronal excitability. We recorded action potential firing from the terminals of individual bronchopulmonary C-fibers using a mouse ex vivo lung-vagal ganglia preparation. C-fibers were characterized as nociceptors or non-nociceptors based upon conduction velocity and response to transient receptor potential (TRP) channel agonists. Antimycin A (mitochondrial complex III Qi site inhibitor) had no effect on the excitability of non-nociceptors. However, antimycin A increased excitability in nociceptive C-fibers: decreasing the mechanical threshold by 50% and increasing the action potential firing elicited by a P2X2/3 agonist to 270% of control. Antimycin A-induced nociceptor hyperexcitability was independent of TRP ankyrin 1 (TRPA1) or TRP vanilloid 1 (TRPV1) channels. Blocking mitochondrial ATP production with oligomycin or myxothiazol had no effect on excitability. Antimycin A-induced hyperexcitability was dependent on mitochondrial ROS and was blocked by intracellular antioxidants. ROS are known to activate protein kinase C (PKC). Antimycin A-induced hyperexcitability was inhibited by the PKC inhibitor bisindolylmaleimide (BIM) I, but not by its inactive analogue BIM V. In dissociated vagal neurons antimycin A caused ROS-dependent PKC translocation to the membrane. Finally, H2O2 also induced PKC-dependent nociceptive C-fiber hyperexcitability and PKC translocation. In conclusion, ROS evoked by mitochondrial dysfunction caused nociceptor hyperexcitability via the translocation and activation of PKC.
Molecular pharmacology.Mol Pharmacol.2014 Mar 18. [Epub ahead of print]
Airway sensory nerve excitability is a key determinant of respiratory disease-associated reflexes and sensations such as cough and dyspnea. Inflammatory signaling modulates mitochondrial function and produces reactive oxygen species (ROS). Peripheral terminals of sensory nerves are densely packed wi
PMID 24642367

Tiotropium modulates transient receptor potential V1 (TRPV1) in airway sensory nerves: A beneficial off-target effect?(⋆).

Birrell MA1, Bonvini SJ1, Dubuis E1, Maher SA1, Wortley MA1, Grace MS1, Raemdonck K1, Adcock JJ1, Belvisi MG2.Author information 1Respiratory Pharmacology, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, United Kingdom.2Respiratory Pharmacology, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, United Kingdom. Electronic address: m.belvisi@imperial.ac.uk.AbstractBACKGROUND: Recent studies have suggested that the long-acting muscarinic receptor antagonist tiotropium, a drug widely prescribed for its bronchodilator activity in patients with chronic obstructive pulmonary disease and asthma, improves symptoms and attenuates cough in preclinical and clinical tussive agent challenge studies. The mechanism by which tiotropium modifies tussive responses is not clear, but an inhibition of vagal tone and a consequent reduction in mucus production from submucosal glands and bronchodilation have been proposed.
The Journal of allergy and clinical immunology.J Allergy Clin Immunol.2014 Mar;133(3):679-687.e9. doi: 10.1016/j.jaci.2013.12.003. Epub 2014 Feb 5.
BACKGROUND: Recent studies have suggested that the long-acting muscarinic receptor antagonist tiotropium, a drug widely prescribed for its bronchodilator activity in patients with chronic obstructive pulmonary disease and asthma, improves symptoms and attenuates cough in preclinical and clinical tus
PMID 24506933

Theophylline inhibits the cough reflex through a novel mechanism of action⋆

Dubuis E1, Wortley MA1, Grace MS1, Maher SA1, Adcock JJ1, Birrell MA1, Belvisi MG2.Author information 1Respiratory Pharmacology, Pharmacology & Toxicology, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, United Kingdom.2Respiratory Pharmacology, Pharmacology & Toxicology, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, United Kingdom. Electronic address: m.belvisi@imperial.ac.uk.AbstractBACKGROUND: Theophylline has been used in the treatment of asthma and chronic obstructive pulmonary disease for more than 80 years. In addition to bronchodilator and anti-inflammatory activity, clinical studies have suggested that theophylline acts as an antitussive agent. Cough is the most frequent reason for consultation with a family doctor, and treatment options are limited. Determining how theophylline inhibits cough might lead to the development of optimized compounds.
The Journal of allergy and clinical immunology.J Allergy Clin Immunol.2014 Jan 7. pii: S0091-6749(13)01781-8. doi: 10.1016/j.jaci.2013.11.017. [Epub ahead of print]
BACKGROUND: Theophylline has been used in the treatment of asthma and chronic obstructive pulmonary disease for more than 80 years. In addition to bronchodilator and anti-inflammatory activity, clinical studies have suggested that theophylline acts as an antitussive agent. Cough is the most frequent
PMID 24406072

Japanese Journal

Pulmonary C-Fibers Do Not Play a Role in Ammonia-Induced Brief Tachypnea in the Rabbit.

MATSUMOTO Shigeji,YAMASAKI Masao,KANNO Takahiro,NAGAYAMA Tadanori,SHIMIZU Tsuyoshi
The Japanese Journal of Physiology 42(3), 377-388, 1992
NAID 130004435434