No abstract

Adenosine deaminase in pleural fluid (pADA), CA125 in serum (sCA125), and IFN-gamma in pleural fluid (pIFN-gamma) were measured in patients with pleurisy of various causes to evaluate their diagnostic utility in tuberculous pleuritis (TBP). We studied 39 pleural fluid samples, including 11 TBP and 28 non-TBP. With both pADA and sCA125, although the median values were much higher in TBP than in non-TBP groups, there was considerable overlap between the two groups. The sensitivity, specificity, and diagnostic efficiency were 81.8%, 89.3%, and 87.2%, respectively, when pADA values of more than 45 U ml-1 were considered, and they were 100%, 75.0%, and 84.2%, respectively, when sCA125 values of more than 35 U ml-1 were considered. In contrast, pIFN-gamma values were significantly higher in TBP patients (5.8 +/- 3.0 IU ml-1; mean +/- S.D.) than those in non-TBP patients (< 0.3 IU ml-1), leading to both a sensitivity and a specificity of 100%.

In this study, bacterial attachment to rat tracheal surface was measured using three nonmucoid strains of Pseudomonas aeruginosa and bacterial growth after binding to tracheal surface was also tested. Brush injury on tracheal surface significantly increased bacterial attachment (1,190 to 1,600%); bacteria binding to brush-injured sites grew more rapidly than either nonbinding bacteria or those on intact trachea. A partial characterization of the binding sites for P. aeruginosa on either intact or injured tracheal surface also was performed. Treatment of injured tracheal surface with metaperiodate significantly inhibited attachment of P. aeruginosa, but trypsin treatment did not. In contrast, neither reagent had any effects on bacterial attachment to intact tracheal surface. These results suggest that brush injury on tracheal surface produces new binding sites as a receptor for P. aeruginosa, and that this receptor has carbohydrates as important components and that it is not a protein receptor. In addition, in order to determine what the dominant sugar of this receptor was, we tested the inhibition of bacterial attachment with monosaccharide, neuraminidase, and lectin. Treatment of bacteria with N-acetylneuraminic acid (NANA) dramatically inhibited bacterial attachment to injured trachea. However, NANA also inhibited the growth of this organism. Moreover, neither neuraminidase nor lectin data suggested that the dominant sugar of the receptor was NANA. Our data go so far as to confirm that the major component of the receptor of nonmucoid strains of P. aeruginosa on brush-injured trachea is carbohydrates; it is still unclear what kind of sugar is the dominant component of the receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this study was to evaluate the effects of bee products such as honey, royal jelly and propolis on 5-fluorouracil-induced experimental oral mucositis in hamsters. Oral mucositis was induced in hamsters through a combination of 5-fluorouracil and mild abrasions that were made on the cheek pouch. Honey, royal jelly and propolis were thereafter topically administered to the oral mucosa, and then the healing process was examined by measuring the size of the mucositis. Honey (1%, 10% and 100%) and propolis (0.3%, 1% and 3%) ointments did not reduce the size of the mucositis in comparison to the vaseline-treated control group. However, the royal jelly (3%, 10% and 30%) ointments significantly improved the recovery from 5-fluorouracil-induced damage in a dose-dependent manner. These results suggest the possibility that the topical application of royal jelly has a healing effect on severe oral mucositis induced by chemotherapy.

This study examines the bronchial alveolar lavage (BAL) samples from a group of patients with acute bacterial pneumonia (n = 13) and makes a comparison with a control group (n = 5). The proteinase inhibitory capacity was examined and found to be composed primarily of alpha 1-proteinase inhibitor (PI, alpha 1-antitrypsin) and, to a lesser extent, bronchial mucosal inhibitor. Although the average PI concentration was elevated approximately 5-fold in the pneumonia group, its inhibitory function against elastase was decreased 15-fold when compared with that in the control group. The pneumonia group showed an increased concentration of immunologically identified elastin-derived peptides. Some of the BAL fluid from patients with pneumonia showed elastolytic activity against amorphous insoluble lung elastin. The majority of the elastase appears to be of neutrophil origin. Bronchial mucosal inhibitor is shown to be a component of both normal and pneumonia BAL fluids by both immunologic quantitation and by its resistance to perchloric acid inactivation. Compared with those from control subjects, BAL samples from patients with acute bacterial pneumonia showed a decreased proteinase inhibitor function and both increased elastolytic activity and elastin-derived peptide concentration.