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Mycobacterium shimoidei (Tsukamura 1982) is an uncommon but widely distributed pathogen usually isolated from respiratory specimens. We report two cases of lung disease due to M. shimoidei and the associated bacteriological results. A 45-year-old man (Case 1) admitted to National Hospital Organization (NHO) Miyagi Hospital, a 75-year-old man (Case 2) admitted to NHO Higashi-Hiroshima Medical Center were found in initial chest X-ray and thoracic computed tomography (CT) to have a tuberculosis-like cavity in the left apex (Case 1) and the right apex (Case 2). In Case 1, the patient was treated with isoniazid and rifampicin for one month and lesions showed a partial response. In Case 2, the patient responded favorably with rifampicin, ethambutol, streptomycin, and clarithromycin therapy. Mycobacteria were repeatedly detected in smear and culture from sputum specimens in both patients. Isolates were nonphotochromogenic and rough. Isolated colonies developed after two to three weeks on 2% Ogawa egg medium. Organisms grew on 2% Ogawa egg medium at 30, 37, 42, and 45 degrees C, but not 25 degrees C. Both organisms were susceptible to 500 microg of p-nitrobenzoate per mL and 5mg of sodium chloride per mL. Isolates were negative for niacin accumulation, nitrate reduction, semiquantitative catalase, 68 degrees C catalase, 3-day aryl-sulfatase, iron uptake, and MPB64 antigen production, but positive for Tween 80 hydrolysis (5 and 10 days), acid phosphatase, and pyrazinamidase. Isolates had typical uv-HPLC chromatograms similar to M. shimoidei, demonstrating triple-peak clusters with peaks in the early cluster. 16S rRNA gene sequencing showed isolates to be consistent with Mycobacterium shimoidei. Based on composite characterization, isolates were identified as M. shimoidei. This is, to our knowledge, the third case of M. shimoidei infection reported in Japan.

Purpose: Nitroglycerin may improve the response to chemotherapy in advanced non-small cell lung cancer. The effects and mechanisms of nitroglycerin on the enhancement of chemosensitivity to docetaxel and carboplatin regimen (DCb) in patients with lung adenocarcinoma have not been reported., Experimental Design: Seventeen patients with operable lung adenocarcinoma and stable angina pectoris were selected to investigate the effects of nitroglycerin on immunoreactivity for hypoxia-inducible factor 1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF), P-glycoprotein (P-gp), the production of which is regulated by HIF-1, and p53 proteins in their resected tumor by semiquantitative immunohistochemical analyses. Eight of 17 patients were treated with nitroglycerin patches before operation, but 9 of 17 patients were not. Furthermore, to study the relationship between changes in plasma VEGF levels by nitroglycerin treatment and response to DCb, 29 patients with advanced lung adenocarcinoma were treated with nitroglycerin for 3 days before chemotherapy using DCb., Results: The rates of immunoreactive cells for HIF-1alpha, VEGF, and P-gp in tumor tissues treated with nitroglycerin were lower than those without nitroglycerin, but those for p53 were not different between those treated with and without nitroglycerin. Furthermore, the rates of immunoreactive cells for VEGF and P-gp proteins were significantly associated with those for HIF-1alpha in tumor tissue. The magnitude of decrease in plasma VEGF levels after treatment with nitroglycerin was significantly associated with response to DCb in patients with advanced lung adenocarcinoma., Conclusions: Nitroglycerin treatment may improve response to DCb in patients with lung adenocarcinoma, partly through decreasing VEGF and P-gp production via reduction of HIF-1alpha.

It is still uncertain how viral respiratory infections cause acute exacerbations of bronchial asthma, although several mechanisms have been proposed. We studied the relationship between the airway narrowing and the inflammatory and bronchospastic factors in peripheral venous blood and urine, in 30 patients with asthma at the exacerbations caused by upper respiratory tract infections (URTIs). Acute exacerbations caused decreases in peak expiratory flow rate (PEFR) in all 30 patients with asthma. Asthma exacerbations caused the rises in serum levels of interleukin-6, soluble intercellular adhesion molecule-1 and eosinophil cationic protein, concentrations of urinary leukotriene E4 and plasma histamine, compared with those in patients with asthma at a stable condition and those in 30 control subjects (p < 0.05). The values of PEFR at the exacerbations correlated with the levels of these factors. Treatment with oral glucocorticoids reversed the decreases in PEFR and the increases in these factors. At the onset of URTIs, rhinovirus and influenza type A virus were identified in 13 and 7 patients, respectively. Each of parainfluenza virus, adenovirus, and enterovirus was identified in one patient. These findings suggest that respiratory viral infections may cause acute asthma exacerbations via the production of mediators that induce inflammation and bronchospasm.

Exhaled carbon monoxide (CO) concentrations were measured on a CO monitor by vital capacity maneuvers in asthmatic patients receiving or not receiving inhaled corticosteroids and in nonsmoking and smoking healthy control subjects. CO was detectable and measured reproducibly in the exhaled air of all subjects. The exhaled CO concentrations were higher in asthmatic patients not receiving inhaled corticosteroids (5.6+/-0.6 ppm, p < 0.001) and similar in asthmatic patients receiving inhaled corticosteroids (1.7+/-0.1 ppm) compared with those in nonsmoking healthy control subjects (1.5+/-0.1 ppm). Smoking healthy control subjects had the highest levels of exhaled CO concentration among the groups (21.6+/-2.8 ppm, p < 0.001). To examine whether inhaling corticosteroids reduce exhaled CO concentration in a given asthmatic patient, 12 patients with symptomatic asthma who were being treated by inhaled beta2-agonists alone underwent measurements of exhaled CO concentration before and 4 wk after the initiation of inhaled corticosteroid treatment. All patients had reductions in exhaled CO concentration (p < 0.001) and eosinophil cell counts in sputum (p < 0.01) that were accompanied by an improvement in airway obstruction. Changes in exhaled CO concentration were significantly related to those in the eosinophil cell counts in sputum (p < 0.001). The present study shows an elevation of exhaled CO in asthmatic patients that decreases with corticosteroid therapy. Increases in the exhaled CO levels therefore may reflect inflammation in the asthmatic lung.