CrossRefPubMed 5. Robins-Browne RM, Hartland EL:Escherichia coli as a cause of diarrhea. J Gastroenterol Hepatol 2002, 17:467–475.CrossRefPubMed 6. Ramachandran V, Brett K, Hornitzky MA, Dowton M, Bettelheim KA, Walker MJ, Djordjevic SP: Distribution of intimin subtypes among Escherichia coli isolates from ruminant and human sources. J Clin Microbiol 2003, 41:5022–5032.CrossRefPubMed 7. Robins-Browne RM, Bordun A-M, Tauschek
M, Bennett-Wood VR, Russell J, Oppedisano F, Lister NA, Bettelheim KA, Fairley CK, Sinclair MI, Hellard ME:Escherichia coli and community-acquired gastroenteritis, Melbourne, Australia. Emerg Infect Dis 2004, 10:1797–1805.PubMed 8. Sethabutr O, Venkatesan M, Yam S, MAPK inhibitor Pang LW, Smoak BL, Sang WK, Echeverria P, Taylor DN, Isenbarger DW: Detection of PCR products of the ipaH gene from Shigella and enteroinvasive Escherichia coli by enzyme-linked immunosorbent assay. Diagn Microbiol Infect Dis 2000, 37:11–16.CrossRefPubMed Vorinostat mouse 9. Gross RJ, Rowe B: Serotype of Escherichia coli. The virulence of Escherichia coli: reviews and methods (Edited by: Sussman M). Academic Press Inc: London 1985.
10. Clinical and Laboratory Standards Institute: Performance standards for antimicrobial susceptibility testing: fifteenth informational supplement. Clinical Laboratory Standards Institute, Wayne, PA 2005. 11. Rotimi VO, Jamal W, Pal T, Sovenned A, Albert MJ: Emergence of CTX-M-15 type extended-spectrum β -lactamase-producing Salmonella spp. in Kuwait and the United Arab Emirates. J Med Microbiol 2008, 57:881–886.CrossRefPubMed 12. World Health Organisation: Programme for control of diarrhoeal diseases (CDD/83.3 Rev 1). Manual for laboratory investigations of acute enteric infections World Health Organisation, Geneva 1987, 27. 13. Levine MM, Edelman R: Enteropathogenic Escherichia coli of classic serotypes associated with infant diarrhea: epidemiology and pathogenesis. Epidemiol Rev 1984, 6:31–51.PubMed 14. Rao MR, ALK inhibitor Abu-Elyazeed R, Savarino SJ, Naficy AB, Wierzba
TF, Abdel-Messih I, Shaheen H, Frenck RW Jr, Svennerholm A-M, Clemens JD: High disease burden of diarrhea due to enterotoxigenic Escherichia coli among rural Egyptian infants and young children. J Clin Microbiol Gefitinib chemical structure 2003, 41:4862–64.CrossRefPubMed 15. Aslani MM, Ahrabi SS, Alikhani YM, Jafari F, Zali RM, Mani M: Molecular detection and antimicrobial resistance of diarrheagenic Escherichia coli strains isolated from diarrheal cases. Saudi Med J 2008, 29:388–392.PubMed 16. Al-Gallas N, Bahri O, Bouratbeen A, Ben Haasen A, Ben Aissa R: Etiology of acute diarrhea in children and adults in Tunis, Tunisia, with emphasis on diarrheagenic Escherichia coli : prevalence, phenotyping, and molecular epidemiology. Am J Trop Med Hyg 2007, 77:571–582.PubMed 17. Porat N, Levy A, Fraser D, Deckelbaum RJ, Dagan R: Prevalence of intestinal infections caused by diarrheagenic Escherichia coli in Bedouin infants and young children in Southern Israel. Pediatr Infect Dis J 1998, 17:482–488.
Figure 1 SEM planar view of an anodic alumina membrane anodized at 130 V. SB525334 Effect of applied voltage To evaluate the effect of anodizing voltage, both the first and the second anodizing steps are carried out by applying similar DC voltages ranging from 100 to 130 V for fix anodizing time of 20 h. This range of voltages
is selected based on our previous observation on the optimized semiconductor activity of the PAAO membranes formed via aluminum anodizing at approximately 115 V for up to about 20 h [10]. Different excitation wavelengths are tested in order to identify most of the details of the subband states. It is observed that under 265-nm excitation wavelength, Cyclosporin A the PL emission includes most of the emission peaks which are observed by exciting the membranes under different excitation wavelengths solely. Hence, our interpretation of the defect-based subband states is CP868596 based on the PL emissions measured under 265-nm excitation. All the measured PL emission spectra of the membranes produced at 100, 115, and 130 V, are presented in Figure 2. It is observed that all the membranes
show PL emission in the 300- to 550-nm wavelength range. Qualitatively, a redshift is observed within some of the measured PL spectra (see Figure 2). It is evident that an increase in anodizing voltage leads to a slight shift in the emission peaks toward the visible region. Thus, the subband gaps present in the electronic structure of the membranes are narrowed slightly by an increase in anodizing voltage. It should be pointed out that the shift rate is much more below 115 V, and it decreases afterward. It could be deduced that in these membranes, an increase in anodizing voltage by approximately 115V enhances formation of optically active defects with subband gaps which lay in the visible range. Figure 2 PL emission spectra of PAAO membranes formed, using different anodizing voltages, in phosphoric acid. The PL emission of metal oxides usually has various origins like intrinsic electronic point defects. It is known that for isolated similar
point defects in an amorphous material, the PL emission has a normal (Gaussian) shaped distribution. In the case of different light-emitting point defects, the PL emission regarding each defect type will contribute Megestrol Acetate to the whole emission spectrum through a Gaussian-like peak. Gaussian fitting analyzes these contributions and assists us to identify different electronic point defects which arise in the PAAO membranes. The analyzed emission spectra of Figure 2 are shown in Figure 3a,b,c. Those figures show that PL emission of all the membranes are composed of five different Gaussian-shaped functions. The Gaussian functions in Figure 3a are fitted to peaks about 361, 381, 415, 453, and 486 nm which correspond to 3.43, 3.25, 2.99, 2.74, and 2.55 eV subband transitions, respectively.