We report on an artificially intelligent nanoarray based on molecularly modified gold nanoparticles and a random network of single-walled carbon nanotubes for noninvasive diagnosis and classification of a number of diseases from exhaled breath. The performance of this artificially intelligent nanoarray was clinically assessed on breath samples collected from 1404 subjects having one of 17 different disease conditions included in the study or having no evidence of any disease (healthy controls). Blind experiments showed that 86% accuracy could be achieved with the artificially intelligent nanoarray, allowing both detection and discrimination between the different disease conditions examined. Analysis of the artificially intelligent nanoarray also showed that each disease has its own unique breathprint, and that the presence of one disease would not screen out others. Cluster analysis showed a reasonable classification power of diseases from the same categories. The effect of confounding clinical and environmental factors on the performance of the nanoarray did not significantly alter the obtained results. The diagnosis and classification power of the nanoarray was also validated by an independent analytical technique, i.e., gas chromatography linked with mass spectrometry. This analysis found that 13 exhaled chemical species, called volatile organic compounds, are associated with certain diseases, and the composition of this assembly of volatile organic compounds differs from one disease to another. Overall, these findings could contribute to one of the most important criteria for successful health intervention in the modern era, viz. easy-to-use, inexpensive (affordable), and miniaturized tools that could also be used for personalized screening, diagnosis, and follow-up of a number of diseases, which can clearly be extended by further development.

Excess of intracellular reactive oxygen species results in an environment that may modulate gene expression, or damage cellular molecules. These events are assumed to contribute to the process of carcinogenesis. In the present study, we measured the extent of lipid peroxidation and antioxidative status in colonic tumors and normal colonic mucosa obtained from 25 patients with colorectal carcinoma. Levels of lipid peroxides (PD) and of thiobarbituric acid reactive substances (TBARS) were significantly increased, by 54 and 59%, respectively, in tissue specimens obtained from the colonic tumor as compared with normal colonic mucosa (PD, 2.78+/-0.31 versus 1.81+/-0.29 nmol/mg tissue, TBARS, 0.86+/-0.1 versus 0.54+/-0.08 nmol/mg tissue). Activities of the antioxidant enzymes catalase and glutathione peroxidase (GPx) were also higher (by 67 and 29%, respectively) than in normal mucosa, probably in response to the increased free radical stress occurring in cancerous tissues. Myeloperoxidase (MPO) and adenosine deaminase (ADA) are markers of activated leukocytes and are related to the production of oxygen free radicals by these cells. Their activities were significantly elevated in the neoplastic tissue as compared to the normal tissue (MPO, 7.4+/-1.5 versus 4.1+/-0.95 U/mg tissue, ADA, 4.17+/-0.65 versus 2.99+/-0.80 U/g tissue), suggesting a possible involvement of activated leukocytes in the enhanced oxidative stress in the cancerous tissue. Our results demonstrate an enhanced oxidative stress in the neoplastic tissue. Leukocyte activation was also higher in the carcinogenic tissue, indicating a possible contribution of these cells to a further oxidative stress-derived tissue injury. These observations add to previous studies and may encourage therapeutic trials with antioxidants as a means of preventing colorectal cancer and preventing further tissue injury in the neoplastic tissue and its surroundings.

Increased oxidative stress has been previously demonstrated in patients with Crohn's disease (CD). However, to date, this parameter has not been assessed in a comparative study of patients in prolonged remission and those with the active disease. We report here our study of lipid peroxidation, antioxidant and inflammation status in serum derived from 16 active CD patients, 27 clinically stable patients, and 15 healthy controls. Results The extent of lipid peroxidation was higher in CD patients than in the healthy controls, while the levels of lipid peroxides (PD) and of thiobarbituric acid-reactive substances (TBARS) were significantly (P < 0.01) higher in serum obtained from patients with active CD (22 and 30%, respectively) than in that obtained from patients in remission. An analysis of the antioxidant status revealed that the beta-carotene levels in sera derived from all CD patients - patients with active or stable CD (49.4 +/- 15 and 95.6 +/- 25 mg% beta-carotene, respectively) - were higher than that in the controls (145 +/- 40 mg%). Serum activity of glutathione peroxidase (GSH-Px) was significantly (P < 0.001) higher (by 31%) in the patients with active CD than in the control group. There was no significant difference in GSH-Px activity between patients in remission and the controls. In terms of the inflammatory status, we found significantly (P < 0.01) higher levels of C-reactive proteins (CRP) and of tumor necrosis factor alpha (TNFalpha) in patients with active CD than in CD patients in remission. There was a significant correlation between those parameters and the extent of lipid oxidation. Neutrophils, which are a potential source of oxygen-free radicals, were activated by incubation with phorbol myristate acetate (PMA). Superoxide and lysozyme release were significantly reduced in neutrophils derived from patients with active CD (by 25 and 28%, respectively) in comparison to the control group. However, stimulated neutrophils from stable patients demonstrated only a minimally non-significant lower release of superoxide and lysozyme compared to the controls. Conclusion The results obtained in this study demonstrate an enhanced inflammatory and oxidative stress and a decreased antioxidant status in patients with active CD. As the patients improved and became clinically stable, the oxidative parameters decreased, approaching normal values. As neutrophil activation was also lower in patients with active disease, neutrophil activation may represent a possible defense mechanism of the body against tissue injury.

The success rate was high with the OTSC system, and it is concluded to be a safe and effective treatment for LSG leaks.