Although it is well recognized that beta-blockers can induce bronchoconstriction only in patients with asthma, mechanisms of the bronchoconstriction are not well known. We hypothesize that bronchoconstriction induced by beta-blockers may result from inflammatory mediators released by allergic reactions. In this study, we developed a guinea pig model for propranolol-induced bronchoconstriction (PIB) after antigen inhalation and investigated the effect of specific thromboxane (TXA2) receptor antagonists, S-1452 and ONO NT-126, on PIB in passively sensitized and artificially ventilated guinea pigs to determine whether TXA2 is involved in PIB. Propranolol caused bronchoconstriction with 10 mg/ml of propranolol was inhaled 20 min after antigen challenge. On the other hand, propranolol did not produce bronchoconstriction after antigen provocation in nonsensitized guinea pigs or after saline provocation in sensitized animals. Pretreatment of the animals with S-1452 in doses of 0.01 and 0.1 mg/kg and ONO NT-126 in doses of 1.0 and 10 micrograms/kg injected intravenously 15 min after antigen challenge as well as before antigen challenge reduced PIB in a dose-dependent manner. Bronchoconstriction caused by methacholine did not induce PIB. These results suggest that TXA2 has an important role in the pathophysiology of the PIB that develops after the allergic bronchoconstriction.

There is no detailed information about benign asbestos pleural effusion (BAPE). The aim of the study was to clarify the clinical features of BAPE. The criteria of enrolled patients were as follows: (1) history of asbestos exposure; (2) presence of pleural effusion determined by chest X-ray, CT, and thoracentesis; and (3) the absence of other causes of effusion. Clinical information was retrospectively analysed and the radiological images were reviewed. There were 110 BAPE patients between 1991 and 2012. All were males and the median age at diagnosis was 74 years. The median duration of asbestos exposure and period of latency for disease onset of BAPE were 31 and 48 years, respectively. Mean values of hyaluronic acid, adenosine deaminase, and carcinoembryonic antigen in the pleural fluid were 39,840 ng/mL, 23.9 IU/L, and 1.8 ng/mL, respectively. Pleural plaques were detected in 98 cases (89.1%). Asbestosis was present in 6 (5.5%) cases, rounded atelectasis was detected in 41 (37.3%) cases, and diffuse pleural thickening (DPT) was detected in 30 (27.3%) cases. One case developed lung cancer (LC) before and after BAPE. None of the cases developed malignant pleural mesothelioma (MPM) during the follow-up.

A total of 152 patients with asbestos-related lung cancer recognized by the criteria of Japanese compensation law for asbestosrelated diseases were examined and compared with 431 patients with non-asbestos-related lung cancer. Male comprised 96% of patients. Ages ranged from 50 to 91 years with a median of 72 years. Eighty-nine percent were smokers or ex-smokers. Almost all patients had occupational histories of asbestos exposure. The median duration of asbestos exposure was 31 years and the median latency period was 47 years. Thirty-four percent of patients exhibited asbestosis and 81% exhibited pleural plaques by radiography. Regarding asbestos particles in the lung for 73 operated or autopsied patients, 62% had more than 5,000 particles per gram. On the other hand, 100% of non-asbestos-related lung cancer patients had <5000 particles per gram with a median of 554 particles. The number of asbestos bodies in the lung, male gender, absence of symptoms, smoking index, and early stage of cancer were significantly much more than those of non-asbestos-related lung cancer. In this study, a diagnosis of asbestos-related lung cancer was made in 34% of patients by asbestosis, in 62% by presence of both pleural plaques and more than 10 years' occupational asbestos exposure, and in 4% by more than 5000 asbestos particles per gram of lung tissue. Occupational histories, duration of asbestos exposure, and pleural plaques are common categories for the recognition of asbestos-related lung cancer in Japan. (Cancer Sci 2010; 101: 1194-1198 T he disaster of asbestos exposure has been a serious social problem in Japan since 2005,(1) with neighborhood exposure to asbestos inducing mesothelioma in more than 100 patients in the Amagasaki area. Furthermore, the number of patients with mesothelioma and asbestos-related lung cancer ( Fig. 1) has recently increased. In this study, clinical features and occupational histories for asbestos-related lung cancer patients in Japan were investigated and compared with those of non-asbestos-related lung cancer patients. Materials and MethodsIn this study, the definition of asbestos-related lung cancer was primary lung cancer with the following: (i) asbestosis on chest radiography; (ii) pleural plaques with more than 10 years' occupational asbestos exposure; (iii) asbestos particles or fibers on the lung tissues with more than 10 years' occupational asbestos exposure; and (iv) more than 5000 asbestos particles per gram of dry lung tissue with occupational asbestos exposure. These criteria fulfill the Japanese compensation law of asbestos-related lung cancer.Retrospective study of asbestos-related lung cancer patients from 2000 to 2008 treated in 18 Rosai hospitals throughout Japan was performed. Gender, age, diagnostic motive, smoking history, histological type of lung cancer, clinical stage, therapeutic procedures and prognosis, occupational history, and radiological findings of asbestos-related changes were examined.Non-asbestos-related lung cancer patients treated in Okayama Rosai hospital fr...

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