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Background: In WDM networks, there is a crucial need to monitor signal degradation factors in order to maintain the quality of transmission. This is more critical in dynamic optical networks as non-linear impairments are network state dependent. Moreover, PLIs are accumulative in nature, so the overall impact is increased tremendously as the length of signal path is increased. The interactions between different impairments along the path also influence their overall impact. Objective: Among the different impairments, the present work focuses on phase modulations owing to the intensities of signals themselves as well as the neighboring signals. It includes the influence of SPM, SPM and XPM, system parameters like signal power, wavelength and fiber parameters like attenuation coefficient, dispersion coefficient and their influence on Q-value and BER. Methods: The analysis is done through a single and two-channel transmitter system with varied power, wavelengths and system parameters. The corresponding optical spectrums are analysed. Results & Conclusion: It has been found that SPM and XPM pose broadening effect on spectrum without any effect on temporal distributions. The magnitude of signal power is among the parameters significantly influencing the broadening of spectrum. The higher the power, the more the magnitude of broadening. It has been found that in order to neglect the impact of input power; its magnitude must be kept below 20 mW. Also, the dispersion and attenuation value need to be carefully as they pose counteracting effect to SPM and XPM for certain values and hence can be used as compensation measures without any additional cost.

Additional file 1: Figure S1. 2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)-N-phenylacetamide (7a). Figure S2. N-(2-fluorophenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7b). Figure S3. N-(4-fluorophenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7c). Figure S4. N-(2-chlorophenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7d). Figure S5. N-(3-chlorophenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7e). Figure S6. N-(4-chlorophenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7f). Figure S7. N-(4-bromophenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7g). Figure S8. 2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)-N-(o-tolyl)acetamide (7 h). Figure S9. 2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)-N-(p-tolyl)acetamide (7i). Figure S10. N-(2,6-dimethylphenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7j). Figure S11. N-(4-ethylphenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7k). Figure S12. 2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)-N-(4-methoxyphenyl)acetamide (7 l). Figure S13. N-(4-hydroxyphenyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7m). Figure S14. 2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)-N-(4-nitrophenyl)acetamide (7n). Figure S15. 2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)-N-(naphthalen-2-yl)acetamide (7o). Figure S16. 2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)-N-(4-methylbenzyl)acetamide (7p). Figure S17. N-(4-fluorobenzyl)-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7q). Figure S18. N-benzyl-2-(2-methoxy-4-(4-oxo-3,4-dihydroquinazolin-2-yl)phenoxy)acetamide (7r).

Pseudomonas aeruginosa as an opportunistic pathogen produces several virulence factors. The most important of these factors are exotoxin A and type III secretion system (T3SS). The aim of this study was to determine the frequency of toxA, exoU and exoS genes among clinical isolates of P. aeruginosa. In this cross-sectional study from September 2011 to February 2012, 156 P. aeruginosa isolates were recovered from different clinical samples. Susceptibility testing against 10 antibiotics was performed on individual isolates by the disc diffusion method according to CLSI guidelines. Extracted DNA was subjected to PCR assay for determining the presence of toxA, exoU and exoS genes. Overall, the frequency of toxA, exoU and exoS genes were 90.4%, 66.7% and 65.4%, respectively. All of the abdominal and eye isolates were exoS (+). The frequency of exoS (+)/exoU (-) and exoS (-)/exoU (+) genotypes was estimated 19.2% and 16.2%, respectively. Indeed, genotypes exoS (+)/exoU (+) and exoS (-)/exoU (-) were found with frequencies of 48.7% and 15.3%, respectively. The highest and lowest antibiotic resistance rate was seen against azteroenam (94.2%) and amikacin (44.9%), respectively. Fluoroqinolone-resistant isolates were isolated with frequency of 45.8%. Multi-drug resistant (MDR) isolates were detected in 62.8% of isolates. The resistance rate in exoU (+) isolates was 86% compared to 66% in exoS (+) isolates. The high frequencies of virulence genes detected in our clinical isolates with notable antibiotic resistance rates indicate the potential risk of these isolates in nosocomial infections.