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Who was Who in Polymer Science: I
No full textImanishi, Yukio Imoto, Minoru Inagaki, Hiroshi Inoue, Shohei Ise, Norio Israel, Stanley Itoh, Yoshikazu Iwakura, Yoshi
Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation
No full text Matsumoto, Koichiro, Hisamichi Aizawa, Hiromasa Inoue, Mutsumi Shigyo, Shohei Takata, and Nobuyuki Hara. Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation. J. Appl. Physiol. 81(6): 2358–2364, 1996.—We investigated the role of neurogenic inflammation and the subsequent mechanisms in cigarette smoke-induced airway hyperresponsiveness in guinea pigs. Exposure to cigarette smoke was carried out at tidal volume for 3 min. Airway responsiveness to histamine was determined before and after smoke exposure followed by bronchoalveolar lavage (BAL). Plasma extravasation was evaluated by measuring the extravasation of Evans blue dye in the airway. Cigarette smoke produced significant airway hyperresponsiveness and plasma extravasation, with an influx of neutrophils in BAL fluid. FK-224 (10 mg/kg iv), a tachykinin antagonist at NK1 and NK2 receptors, significantly inhibited these changes. The thromboxane (Tx) B2 concentration was increased in BAL fluid after smoke exposure and was significantly inhibited by FK-224. OKY-046 (10 mg/kg iv), a Tx synthase inhibitor, significantly inhibited airway hyperresponsiveness but had no effect on neutrophil influx or plasma extravasation. The results suggest that neurogenic inflammation and the subsequent generation of Tx in the airway are important in the development of the airway hyperresponsiveness induced by cigarette smoke. </jats:p
Nitric oxide derived from sympathetic nerves regulates airway responsiveness to histamine in guinea pigs
No full text Matsumoto, Koichiro, Hisamichi Aizawa, Shohei Takata, Hiromasa Inoue, Naotsugu Takahashi, and Nobuyuki Hara.Nitric oxide derived from sympathetic nerves regulates airway responsiveness to histamine in guinea pigs. J. Appl. Physiol. 83(5): 1432–1437, 1997.—Nitric oxide (NO), which can be derived from the nervous system or the epithelium of the airway, may modulate airway responsiveness. We investigated how NO derived from the airway nervous system would affect the airway responsiveness to histamine and acetylcholine in mechanically ventilated guinea pigs. An NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) (1 mmol/kg ip) significantly enhanced airway responsiveness to histamine but not to acetylcholine. Its enantiomerd-NAME (1 mmol/kg ip), in contrast, had no effect. Thel-NAME-induced airway hyperresponsiveness was still observed in animals pretreated with propranolol (1 mg/kg iv) and atropine (1 mg/kg iv). Pretreatment with the ganglionic blocker hexamethonium (2 mg/kg iv) completely abolished enhancing effect of l-NAME on airway responsiveness. Bilateral cervical vagotomy did not alter thel-NAME-induced airway hyperresponsiveness, whereas sympathetic stellatectomy completely abolished it. Results suggest that NO that was presumably derived from the sympathetic nervous system regulates airway responsiveness to histamine in guinea pigs. </jats:p
Primary adenocarcinoma of the female urethra: report of a case
No full textA case of primary adenocarcinoma of the female urathra was reported. The patient was a 71-year-old female who came with the chief complaint of dysuria. Bilateral cutaneous ureterostomy and ligation of internal iliac arteries were done. Three weeks later, total cystourethrectomy with partial resection of the anterior vaginal wall and dissection of the pelvic lymphnodes, were performed. Histological study of the removed specimen revealed the tubular and mucus-secreting adenocarcinoma, site of origin being paraurethral glands. Fourteen months after surgery, she died of the pulmonary metastasis
Studies on Syntheses and Reactions of Macromolecular Compounds Related to Biochemical Reactions
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