Semiconductor-assisted photodegradation of lignin, dye, and kraft effluent by Ag-doped ZnO.

This work reports a preliminary study of semiconductor-assisted photochemical degradation of lignin, Remazol Brilliant Blue R and Kraft E1 paper effluent by using ZnO and Ag-doped ZnO photocatalysts. The doped semiconductor was prepared in the reaction media by photoreduction of silver nitrate. With the use of 100 mg of ZnO and 15 mg of Ag-ZnO, almost total decolorization of the dye and lignin samples in reaction times lower than 60 min were observed. Extending the photochemical reaction up to 120 min, the total organic carbon content (TOC) was reduced in 90%. For the paper effluent, a fast decolorization was obtained for relatively short reaction times. However, de TOC reduction was negligible (near of 10%) up to high reaction times (300 min). By using the Ag-ZnO photocatalyst, the toxicity of lignin and Kraft E1 effluent toward E. Coli was completely removed. For the dye, the formation of transient toxic species was observed.

Semiconductor-assisted photocatalytic degradation of reactive dyes in aqueous solution.

This work reports the semiconductor-assisted photochemical degradation of reactive dyes. In an oxygenated-UV-ZnO system almost total decolorization of Remazol Brilliant Blue R, Remazol Black B, Reactive Blue 221 and Reactive Blue 222 was observed in reaction times of about 60 min. Extending the photochemical treatment up to 120 min, mineralization higher than 80% for all the dyes was observed. During the same period, the residual acute toxicity was significantly reduced only for Remazol Black B. A systematic optimization study carried out by factorial design showed that for the reactive dyes tested, the ZnO semiconductor exhibits a better efficiency than that observed with anatase TiO2. A synergistic effect in the coupled TiO2-ZnO system was not observed.

Urinary tract infection in men with AIDS.

OBJECTIVE--To investigate whether bacteriuria and, specifically, symptomatic urinary tract infection (UTI) occur with increased frequency in men with HIV infection. METHODS--In this cross-sectional study we investigated three groups of men, aged from 18 to 50 years. Group A was composed of patients with a diagnosis of AIDS; Group B, of patients without HIV infection, and group C of patients with asymptomatic HIV infection. Patients with any known predisposing factor for UTI were excluded from the study. A clean-catch midstream urine sample was collected from each patient on the first day of hospital admission (groups A and B) or during a visit to the outpatient clinic (group C). Bacteriuria was diagnosed when > or = 100,000 colony forming units/ml, urine were grown. RESULTS--There were 415 patients, 151 in group A, 170 in group B and 94 in group C. Bacteriuria was significantly more frequently in group A (20 cases, 13.3%) than in groups B (3 cases, 1.8%, p = 0.00007) and C (3 cases, 3.2%, p = 0.009). Ten cases of bacteriuria in group A (6.6%) were symptomatic while no case of symptomatic UTI was seen in groups B (p = 0.0004) and C (p = 0.008). The frequency of UTI in homosexual men with AIDS (7 cases, 6.7%) was not significantly different from that observed in men with AIDS who denied homosexuality (3 cases, 6.5%). E coli was the predominant pathogen associated with UTI. Although adequate response to a two-week course of antibiotics was observed in most cases, an in-hospital mortality rate of 20% was found among AIDS patients with symptomatic UTI. CONCLUSIONS--In the present study, the frequency of bacteriuria and symptomatic UTI was found to be increased in men with AIDS. E coli was the predominant pathogen in these cases. These data suggest that symptomatic UTI may represent a relevant cause of morbidity for men with AIDS.