Universities and tobacco money. Japan has laundered tobacco money.
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Biomedical subjects
Publications and source records attributed to H Kawane.
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The measurement of serum (1-3)-beta-D-glucan (beta-glucan) in cases with deep seated mycosis is a useful diagnostic method. Beta-glucan has usually been measured using two different methods: by an alkali treatment, chromogenic automated kinetic assay (chromogenic assay), and by detergent dilution and heating methods, kinetic turbidimetric assay (turbidimetric assay). However, there are often large discrepancies in the beta-glucan values measured by these two methods. In this study, we reexamined the values of beta-glucan obtained by the two techniques, using 343 serum samples from 146 patients who had been treated in Kawasaki Medical School between January 1999 and May 1999, and then analyzed the reasons for the differences. Serum beta-glucan results measured were evaluated by segregating them into three clinical categories: cases with proven deep mycosis, cases with probable deep mycosis and cases without deep mycosis. In addition, the beta-glucan in the samples was suppressed by carboxy-methylated curdlan (CM-curdlan), and then was remeasured to find a non-specific reaction. Although a certain correlation was found between the serum beta-glucan results measured by the two methods, the values measured by the chromogenic assay were, in general, higher than those measured by the turbidimetric assay. There were also many samples in the cases without deep mycosis that showed positive values with the chromogenic assay, but not with the turbidimetric assay. With the turbidimetric assay, the addition of CM-curdlan suppressed the values of beta-glucan in all samples; however, when measured by the chromogenic assay the values in many samples remained high. These results suggest that a non-specific reaction which did not include beta-glucan was detected by the chromogenic assay. Further studies are needed to evaluate the characteristics and comparable usefulness of the two assays.
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Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease (COPD). Smokers have higher death rates for COPD and they also have a higher prevalence of lung function abnormalities. Smoking is associated with a greater annual rate of decline in forced expiratory volume in one second (FEV1). Smoking cessation results in an attenuation of the excessive rates of lung function loss. Patients who stop smoking are likely to survive longer than those who continue to smoke. Smoking cessation is the most important intervention in COPD.
BACKGROUND: Chlamydia pneumoniae is a frequent causative agent of acute respiratory disease and has been recently reported as a possible cause of asthma. OBJECTIVE: We assessed the prevalence of C. pneumoniae infections in adult patients with acute exacerbations of asthma. METHODS: One hundred sixty-eight adult patients with acute exacerbations of asthma and 108 control subjects matched for age, sex, and smoking status were studied. Nasopharyngeal swab specimens were obtained from all subjects and analyzed by isolation in cell culture and polymerase chain reaction (PCR) test for C. pneumoniae. Serum samples were also obtained and tested for C. pneumoniae-specific antibodies by the microimmunofluorescence test. RESULTS: C. pneumoniae was isolated from two (1.2%) asthma patients and none from controls and detected by PCR from nine (5.4%) cases and one (0.9%) control. Both culture positive specimens were also positive in PCR. Further, serologic evidence of acute C. pneumoniae infection was present in 15 (8.9%) of asthma patients and in three (2.8%) of controls (P = .048). The prevalence of C. pneumoniae-specific IgG and IgA was significantly higher in asthma cases than in controls (IgG > or = 1:16: 85.1% versus 67.6%, P = .001; IgA > or = 1:16: 47.6% versus 16.7%, P < .001). Mean titer of IgG and IgA was also significantly greater in asthma cases than in controls (IgG: 38.8 versus 18.1, P = .0001; IgA: 17.2 versus 6.1, P = .0001). CONCLUSIONS: Our data suggest that C. pneumoniae infection may trigger acute exacerbations of adult asthma.
STUDY OBJECTIVES: To determine the possible association of Chlamydia pneumoniae infection with diffuse panbronchiolitis (DPB) and with COPD. DESIGN: Prospective case-control study. SETTING: Division of Respiratory Diseases, Kawasaki Medical School Hospital. PARTICIPANTS: Fifteen DPB and 77 COPD patients who had acute exacerbations of respiratory conditions and 35 and 120 control subjects, respectively, matched for age, sex, and smoking status. MEASUREMENTS AND RESULTS: Nasopharyngeal swabs and paired serum samples were obtained from all patients and control subjects for isolation and antibody testing of C pneumoniae. C pneumoniae was isolated from one DPB patient and from no COPD patients or control subjects. Serologic evidence of acute C pneumoniae infection was observed in one DPB patient (6.7%) and six COPD patients (7.8%). The prevalence and mean titer of C pneumoniae IgG and IgA antibodies were significantly higher in COPD patients than in control subjects (p<0.001). However, no such differences were observed between DPB patients and control subjects. CONCLUSIONS: This study showed that C pneumoniae infection may be associated with acute exacerbations of COPD and that chronic C pneumoniae infection is common in COPD but not in DPB.
We experienced adverse reactions to antituberculous agents in 17 patients (53%) out of 32 patients treated for tuberculosis and nontuberculous pulmonary mycobacteriosis. Side effects were seen in 15 patients (47%), and abnormal laboratory findings were observed in 9 patients (28%). Most side effects mostly appeared within two weeks after the administration, and were of short duration. However, there were also side effects such as neurological symptoms, arthralgia, and general fatigue which appeared after one month and lasted for a long duration. These results suggest that careful observation for adverse reactions in antituberculous treatment is required. Finally, 11 patients with adverse reactions were successfully treated by changing antituberculous agents or readministration after temporary stop of the administration. Four patients improved even with continued use of agents causing side-effects. However, in the case of two patients who had to change antituberculous agents, adverse reactions to all antituberculous agents appeared and the treatment for tuberculosis and nontuberculous pulmonary mycobacteriosis had to be stopped.
We report on two patients with sulbactam/ampicillin (SBT/ABPC)-induced pneumonitis. Both patients were being treated with SBT/ABPC for respiratory-tract infections. Following the initiation of SBT/ABPC chemotherapy, however, chest X-ray films showed a shift of shadow in patient 1 and new pulmonary infiltration shadows in patient 2. Bronchoalveolar lavage fluid (BALF) findings showed a marked increase in the total cell count and percentage of eosinophils in patient 1 and of lymphocytes in patient 2. The results of lymphocyte stimulation tests were SBT/ABPC positive for both patients. SBT/ABPC therapy was therefore discontinued and corticosteroid therapy started. Both patients were subsequently relieved of their symptoms demonstrated significantly lower and pulmonary infiltrate levels. Based on these findings, both patients were given a diagnosis of SBT/ABPC-induced pneumonitis. It has been widely reported that CD 4/CD 8 ratio in BALF decreases in cases of drug-induced pneumonitis. However, some reports have cited increase in the CD 4/CD 8 ratio. In our two patients as well, the CD 4/CD 8 ratio increased. These results, together with the findings from several other case reports, indicate that the CD 4/CD 8 ratio may not be good basis for diagnosing drug-induced pneumonitis. Recently, the incidence of drug-induced pneumonitis has been rising. To our knowledge this is the first report documenting cases of SBT/ABPC-induced pneumonitis.
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Cunninghamella bertholletiae, a rare causative agent of human deep seated mycosis, has been reported with increased frequency in the Western countries, in recent years. We experienced a case of Cunninghamella bertholletiae pulmonary infection in a 63-year-old male with pulmonary fibrosis and mild diabetes mellitus. In spite of intensive anti-fungal chemotherapy following clinical diagnosis, he died of exacerbation of the underlying diseases. Postmortem examination showed Cunninghamella infection in the cavity of the lung and massive pulmonary fibrosis. There was no fungal invasion outside the cavity. This is the third report of Cunninghamella human infection in Japan.
Between 1984 and September 1995, we prescribed home oxygen therapy for 155 patients (96 men and 59 women), mean age 68.6 years) with chronic respiratory failure. Here we describe the underlying diseases, laboratory findings (arterial blood gas analysis and pulmonary-function tests), and outcomes. We also report differences between those who were of least 70 years old (n = 82) and those less than 70 years old (n = 73). The underlying diseases were chronic obstructive pulmonary disease in 55 patients, lung cancer in 33, old pulmonary tuberculosis in 29, and pulmonary fibrosis in 27. Chronic obstructive pulmonary disease, especially pulmonary emphysema, was the most frequently encountered underlying disease in the older patients, whereas pulmonary fibrosis and lung cancer were most common in the younger patients. The duration of observation ranged from less than 1 month to 10 years. At the time of this study 82 patients had died, 31 were still being treated as outpatients at our hospital, 32 had transferred to other hospitals, and the status of 10 patients was unknown. The older and younger patients did not differ with regard to arterial blood gases, pulmonary function at the time home oxygen therapy began, or outcome: We believe that home oxygen therapy was very beneficial in these patients with chronic respiratory failure, because their quality of life improved after the start of this therapy.
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Four cases of pulmonary tuberculosis resembling pulmonary abscess radiographically were reviewed from their clinical features, chest X-ray and chest CT, and the mechanism of formation of so-called niveau-like shadows was discussed. Only one case showed a newly formed tuberculous cavity with air fluid level on chest X-ray, however, even in this case, the possibility of the infection with tubercle bacilli of an emphysematous bulla of the lung could not be completely excluded as several bulla were found on chest CT. The remaining three cases showed a slightly different mechanism of the formation of niveau-like shadows. Namely, mycobacterium tuberculosis spread into an existed bulla and a tubercle bacilli infected bulla was formed. Regarding the clinical features, no remarkable findings were detected and we could find no differences with common tuberculosis. Based on these experiences, the presence of pulmonary tuberculosis resembling the shadow of pulmonary abscess should be emphasized.
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